PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
24081657-5	2014	Using siRNA in cultured human umbilical vein ECs and human pulmonary artery ECs, depletion of Galpha12 and soluble N-ethylmaleimide-sensitive-fusion factor attachment protein alpha (alpha-SNAP), but not Galpha13, inhibited both basal and thrombin-induced vWF secretion, whereas overexpression of activated Galpha12 promoted vWF secretion.	Ethylmaleimide	115-131	coagulation factor II, thrombin	Homo sapiens	238-246	
3026330-5	1986	Additionally, the thiol reagent N-ethylmalemide (NEM) at rather low concentrations abolished thrombin- and adrenaline-induced stimulation of GTP hydrolysis was decreased by only 30-40% by treatment of platelet membranes with even high concentrations of NEM.	Ethylmaleimide	49-52	coagulation factor II, thrombin	Homo sapiens	93-101	
6437813-9	1984	Finally, the thrombin inhibition of human platelet adenylate cyclase was impaired or abolished by Mn2+ and by treatment of the platelet membranes with N-ethylmaleimide or pertussis toxin.	Ethylmaleimide	151-167	coagulation factor II, thrombin	Homo sapiens	13-21	
10487531-0	1999	N-ethylmaleimide inhibition of thrombin-induced platelet aggregation.	Ethylmaleimide	0-16	coagulation factor II, thrombin	Homo sapiens	31-39	
10713553-0	2000	N-Ethylmaleimide induces disaggregation of platelets preaggregated by ADP and thrombin and decreases cytoplasmic calcium level.	Ethylmaleimide	0-16	coagulation factor II, thrombin	Homo sapiens	78-86	
10713553-1	2000	The effect of N-ethylmaleimide (NEM, 1-200 microM) on ADP- and thrombin-induced platelet aggregation and thrombin-induced increase in intracellular Ca2+ concentration was studied.	Ethylmaleimide	32-35	coagulation factor II, thrombin	Homo sapiens	63-71	
10487531-1	1999	The data presented in this report show that N-ethylmaleimide (NEM) is a powerful inhibitor of thrombin-induced platelet aggregation.	Ethylmaleimide	44-60	coagulation factor II, thrombin	Homo sapiens	94-102	
10487531-1	1999	The data presented in this report show that N-ethylmaleimide (NEM) is a powerful inhibitor of thrombin-induced platelet aggregation.	Ethylmaleimide	62-65	coagulation factor II, thrombin	Homo sapiens	94-102	
10487531-4	1999	NEM dose dependently blocked the thrombin-stimulated, but not the phorbol myristate acetate-dependent phosphorylation of the protein kinase C substrate pleckstrin.	Ethylmaleimide	0-3	coagulation factor II, thrombin	Homo sapiens	33-41	
7849614-0	1994	N-ethylmaleimide inhibits platelet aggregation and potentiates hydrogen peroxide formation induced by thrombin.	Ethylmaleimide	0-16	coagulation factor II, thrombin	Homo sapiens	102-110	
8569706-3	1996	Most of the receptor-activated GTPase, stimulated by both thrombin and SFLLRNP in platelet membranes, was inhibited by prior treatment with pertussis toxin or N-ethylmaleimide, suggesting that under these conditions much of the thrombin receptor-stimulated GTPase in platelet membranes is a member of the pertussis toxin-sensitive G alpha i family.	Ethylmaleimide	159-175	coagulation factor II, thrombin	Homo sapiens	58-66	
8569706-3	1996	Most of the receptor-activated GTPase, stimulated by both thrombin and SFLLRNP in platelet membranes, was inhibited by prior treatment with pertussis toxin or N-ethylmaleimide, suggesting that under these conditions much of the thrombin receptor-stimulated GTPase in platelet membranes is a member of the pertussis toxin-sensitive G alpha i family.	Ethylmaleimide	159-175	coagulation factor II, thrombin	Homo sapiens	228-236