PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
7671799-6	1995	The increase in c-Fos immunoreactivity and BDNF mRNA levels by GABA were dependent upon the activation of voltage-gated Ca2+ channels, as shown using the L-type specific Ca2+ channel blocker nifedipine.	Nifedipine	191-201	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	16-21	
8040263-7	1994	Phenylephrine-induced c-fos mRNA was partially inhibited by H-7, a protein kinase C inhibitor, and by nifedipine, a Ca2+ channel blocker; these two compounds together had additive effects.	Nifedipine	102-112	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	22-27	
17913375-7	2007	Prolonged expression of c-Fos was not observed following coadministration of nifedipine and a dopamine D(1) (DA D(1)) receptor agonist, SKF 81297, but could be mimicked by the DA D(2/3) receptor antagonist raclopride, suggesting that the phenomenon is likely related to DA D(2) receptor antagonism.	Nifedipine	77-87	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	24-29	
9737720-7	1998	A role for Ca2+ signaling is inferred, since the L-type Ca2+ channel blocker nifedipine markedly reduces the induction of c-fos and nur-77 by glucose and GLP-1.	Nifedipine	77-87	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	122-127	
12508050-17	2003	In normal myotubes, 10 micro M nifedipine, but not ryanodine, inhibited c-jun and c-fos mRNA increase after K(+) depolarization.	Nifedipine	31-41	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	82-87	
10514457-3	1999	Blockade of calcium influx through nifedipine-sensitive voltage-gated calcium channels reduced buserelin-induced activation of extracellular signal-regulated kinase (ERK) and c-Fos while activation of c-Jun N-terminal kinase and c-Jun was unaffected.	Nifedipine	35-45	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	175-180	
9426840-0	1998	Expression of c-Fos protein immunoreactivity in rat brain during ethanol withdrawal is prevented by nifedipine.	Nifedipine	100-110	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	14-19	
9764482-4	1998	An L-type calcium channel blocker, nifedipine, also inhibited the electrically induced calcium influx and c-fos expression.	Nifedipine	35-45	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	106-111	
9502114-3	1998	The VIP-induced c-fos expression was inhibited in the presence of EGTA, or the L-type Ca2+ channel blockers verapamil and nifedipine.	Nifedipine	122-132	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	16-21	
9426840-3	1998	Intraperitoneal injection of the calcium channel antagonist nifedipine (3 x 100 mg/kg) prior to, and during ethanol withdrawal totally prevented c-Fos protein-like expression.	Nifedipine	60-70	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	145-150	
9462893-14	1997	Nifedipine was found to suppress both Ang II-induced corticosterone release and c-fos expression in the following areas: organum vasculosum of the lamina terminalis (OVLT), median preoptic nucleus (MNPO), hypothalamic paraventricular nucleus (PVN) and supraoptic nucleus (SON).	Nifedipine	0-10	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	80-85