PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
11244024-3	2001	Previously we showed that pressure-induced c-fos expression in intact cannulated rat mesenteric small arteries was inhibited by genistein, a general tyrosine kinase inhibitor.	Genistein	128-137	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	43-48	
12174389-11	2002	The intensity of c-fos, c-jun and cyclin D(1) expression of HSCs treated with 10(-7)mol/L genistein for 48 h was also significantly decreased compared with the controls.	Genistein	90-99	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	17-22	
12174389-12	2002	CONCLUSION: Genistein influences proliferation of HSC, suppresses the expression of alpha-SMA in HSC and t inhibits the intensity of c-fos, c-jun and cyclin D(1) expression of HSCs.	Genistein	12-21	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	133-138	
10406836-11	1999	The pressure-induced expression of c-fos was not inhibited by nitrendipine (10 micromol/L), a calcium-free Krebs" solution containing EGTA (1 to 2 mmol/L), calphostin C (0.1 micromol/L), or cytochalasin D (0.4 micromol/L) but was inhibited by genistein (30 micromol/L).	Genistein	243-252	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	35-40	
10406836-0	1999	Genistein inhibits pressure-induced expression of c-fos in isolated mesenteric arteries.	Genistein	0-9	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	50-55	
9039826-8	1997	Genistein (750 microg/g) induced the uterine expression of c-fos.	Genistein	0-9	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	59-64	
9528974-7	1998	Quantitative solution hybridization analysis revealed a transient increase in c-fos mRNA levels by 20-fold following 30-45 min of LIF treatment, an effect that was inhibited by the tyrosine, as well as serine/threonine kinase inhibitors, genistein, and H7.	Genistein	238-247	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	78-83	
8060343-3	1994	We find that genistein treatment prevents phenylephrine-induced activation of three promoters (Fos, atrial natriuretic factor, ANF, and the myosin light chain 2, MLC-2), which are activated in the hypertrophic response.	Genistein	13-22	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	95-98	
8864900-7	1996	Genistein at 100 micrograms/ml also blocked both bFGF- and PMA-induced increases in c-fos mRNA.	Genistein	0-9	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	84-89	
9067632-3	1997	Similar to IgE-mediated cell degranulation we demonstrated inhibition of the c-fos signal in the absence of calcium and after preincubation of cells with the protein tyrosine kinase inhibitor genistein.	Genistein	192-201	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	77-82	
8625905-9	1996	To determine if addition of genistein to FRTL-5 cells resulted in a general inhibition of Bu2cAMP-induced responses, we examined its effect on the Bu2cAMP-induced increase in c-fos mRNA levels.	Genistein	28-37	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	175-180	
1445353-7	1992	In the presence of 10 microM genistein and 1 mM NiCl2, PDGF induced c-fos and c-myc mRNA, although the [Ca2+]i elevation could be completely blocked by these two agents.	Genistein	29-38	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	68-73	
7835407-9	1994	H7 (50 microM), genistein (2 microM) and okadaic acid (20 nM), all block the induction of c-jun and c-fos mRNA accumulation in the H2O2-treated rat lenses.	Genistein	16-25	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	100-105