PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
12524425-4	2003	In rat or human artery smooth muscle cells, sodium nitroprusside or 8-(2-chlorophenylthio)-cGMP induced a rise in RhoA mRNA and protein expression, which was inhibited by the cGMP-dependent protein kinase (PKG) inhibitor (R(p))-8-bromo-beta-phenyl-1,N(2)-ethenoguanosine 3":5"-phosphorothioate.	Nitroprusside	44-64	protein kinase cGMP-dependent 1	Homo sapiens	206-209	
28480509-8	2018	Sodium nitroprusside, an NO donor, diminished the ox-LDL-mediated activation of ENaC, and this effect was abolished by inhibiting soluble guanylate cyclase (sGC) and PKG.	Nitroprusside	0-20	protein kinase cGMP-dependent 1	Homo sapiens	166-169	
15505114-5	2004	Pressure drops in response to intracarotid bolus application of the NO donor sodium nitroprusside (SNP) were almost abolished in cGKI-/- mice, whereas ACh-induced pressure decreases remained intact in cGKI-/- and eNOS-/- mice.	Nitroprusside	77-97	protein kinase cGMP-dependent 1	Homo sapiens	129-133	
9421291-2	1997	It has been suggested that activation of cyclic GMP-dependent protein kinase (PKG) is a necessary step in the chain of events leading to the production of negative inotropy by muscarinic receptor agonists in mammalian ventricles, and that some cyclic GMP-elevating agents, such as sodium nitroprusside (SNP), fail to exert a negative inotropic effect because they elevate cyclic GMP levels in a pool that does not activate the kinase.	Nitroprusside	281-301	protein kinase cGMP-dependent 1	Homo sapiens	78-81	
12011581-9	2002	Treatment of the PKG-expressing SMC with nitroprusside resulted in phosphorylation of HSP20.	Nitroprusside	41-54	protein kinase cGMP-dependent 1	Homo sapiens	17-20	
11696008-2	2001	The NO donor, sodium nitroprusside (SNP), stimulated PDE5 phosphorylation and activity, which was blocked by the selective PKG inhibitor, KT5823, resulting in an elevation of cGMP levels.	Nitroprusside	14-34	protein kinase cGMP-dependent 1	Homo sapiens	123-126	
11668033-4	2001	In intact muscle cells, low concentrations (10 nM) of isoproterenol and sodium nitroprusside (SNP) inhibited agonist-induced, IP(3)-dependent Ca(2+) release and muscle contraction via PKA and PKG, respectively.	Nitroprusside	72-92	protein kinase cGMP-dependent 1	Homo sapiens	192-195	
11262387-0	2001	A catalytically inactive mutant of type I cGMP-dependent protein kinase prevents enhancement of large conductance, calcium-sensitive K+ channels by sodium nitroprusside and cGMP.	Nitroprusside	148-168	protein kinase cGMP-dependent 1	Homo sapiens	42-71	
11262387-4	2001	We observed that co-transfection of cells with BK(Ca) channels and a catalytically inactive ("dead") mutant of human cGKIalpha prevented enhancement of BK(Ca) channel in response to either sodium nitroprusside or dibutyryl cGMP in a dominant negative fashion.	Nitroprusside	189-209	protein kinase cGMP-dependent 1	Homo sapiens	117-126	
10196172-8	1999	The stimulatory effect of sodium nitroprusside was inhibited by the PKG-inhibitor KT5823.	Nitroprusside	26-46	protein kinase cGMP-dependent 1	Homo sapiens	68-71