PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
9113418-6	1997	Genistein, a potent inhibitor of protein tyrosine kinases, significantly blunted the hydrogen peroxide-induced FGFR1 tyrosine phosphorylation, ERKs activation and c-fos and c-jun expression.	Genistein	0-9	Fos proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	163-168	
8298195-0	1993	Differential regulation of early response genes and cell proliferation through the human granulocyte macrophage colony-stimulating factor receptor: selective activation of the c-fos promoter by genistein.	Genistein	194-203	Fos proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	176-181	
8662783-8	1996	However, stimulation of c-fos was slightly more sensitive to genistein, while the B2 receptor mRNA was more sensitive to inhibition by the protein kinase C inhibitor, calphostin C. The increase in cell surface B2 receptors were functionally coupled to an increase in phosphoinositide-specific phospholipase C, and the effects of PDGF were selective as there was no increase in either angiotensin II- or arginine vasopressin-induced inositol phosphate formation or intracellular calcium release.	Genistein	61-70	Fos proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	24-29	
8675228-12	1996	Using the tyrosine kinase inhibitor genistein (10 microM) a complete inhibition of IL-10 induced c-fos expression was observed.	Genistein	36-45	Fos proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	97-102	
7968349-9	1994	H-7 (50 microM) and genistein (100 microM) blocked c-fos induction as did PKC down-regulation with chronic treatment of phorbol 12-myristate 13-acetate.	Genistein	20-29	Fos proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	51-56	
23614275-13	2013	The expression of C-JUN and C-FOS was higher in keloid fibroblasts treated with 370 microM genistein and lower in keloid fibroblasts treated with 37 microM genistein.	Genistein	156-165	Fos proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	28-33	
23614275-5	2013	The aim of the study was to investigate genistein as a potential regulator of C-JUN, C-FOS and FOS-B of AP-1 subunits expression in skin keratinocytes, fibroblasts and keloid fibroblasts cultured in vitro.	Genistein	40-49	Fos proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	85-90	
23614275-10	2013	Genistein in 370 microM concentration inhibited C-FOS expression in fibroblasts, whereas in 370 and 37 microM concentration genistein inhibited FOS-B expression in keratinocytes.	Genistein	0-9	Fos proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	48-53	
23614275-11	2013	Furthermore, genistein was able to modulate C-JUN and C-FOS genes expression in keloid fibroblasts cultured in vitro.	Genistein	13-22	Fos proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	54-59	
23614275-12	2013	In these cells, transcriptional activity of C-JUN and C-FOS expression depended on employed concentration of genistein.	Genistein	109-118	Fos proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	54-59	
23614275-13	2013	The expression of C-JUN and C-FOS was higher in keloid fibroblasts treated with 370 microM genistein and lower in keloid fibroblasts treated with 37 microM genistein.	Genistein	91-100	Fos proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	28-33	
1382409-3	1992	Pretreatment of cells with genistein or methyl-2,5-dihydroxycinnamate (tyrosine kinase inhibitors) or staurosporine (a protein kinase C inhibitor) for 20 min abolished the c-fos expression induced by PAF.	Genistein	27-36	Fos proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	172-177	
11506505-10	2001	The results suggest that induction of apoptosis, G2 cell cycle arrest and inhibition of c-fos expression, AP-1 transactivation and ERK phosphorylation may contribute to the growth-inhibitory effect of genistein in some breast cell types, but none of these effects of genistein constitutes a generic mode of growth-arresting action.	Genistein	201-210	Fos proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	88-93	
18224451-9	2008	Genistein also up-regulated steady-state levels of both c-Jun and c-Fos.	Genistein	0-9	Fos proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	66-71	
15611796-3	2005	Herein, we demonstrate that the phenotype of T24 cells could be dramatically reversed and became relatively susceptible to growth inhibition by genistein if the synthesis of H-Ras(val 12) or its downstream effector c-Fos had been suppressed.	Genistein	144-153	Fos proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	215-220	
13129470-13	2003	A decline in genistein concentration by about 52 and 56 % over the 120 h culture period was observed with the addition of glucose or FOS to the basal medium (P<0.01), compared with about 91 % loss of genistein in the vessels containing Novasoy (ADM Neutraceuticals) only.	Genistein	13-22	Fos proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	133-136	
13129470-14	2003	Similar trends were obtained using a three-stage chemostat (gut model), in which once again the degradation of genistein was about 22 % in vessel one, about 24 % in vessel two and about 26 % in vessel three in the presence of FOS, compared with a degradation of genistein of about 67 % in vessel one, about 95 % in vessel two and about 93 % in vessel three in the gut model containing Novasoy (ADM Neutraceuticals) only.	Genistein	111-120	Fos proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	226-229	
11506505-8	2001	Cells differed in their susceptibility towards inhibition by genistein of phorbol ester-induced proto-oncogene c-fos levels, transcription factor activator protein-1 (AP-1) activity and extracellular signal-regulated kinase (ERK) activity.	Genistein	61-70	Fos proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	111-116	
16619504-6	2006	Treatment of the non-neoplastic, immortalized human breast epithelial MCF-10F cells with these low concentrations of genistein was associated with decreased cell proliferation, down-regulation of the protooncogene MET, up-regulation of the breast tumor suppressor gene EGR-1, and up-regulation of the immediate-early response genes FOS and JUN.	Genistein	117-126	Fos proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	332-335	
15090535-2	2004	Using c-fos proto-oncogene expression as an early molecular sensor of estrogen action in ERalpha-positive MCF7 and ER-negative SKBR3 breast cancer cells, we have discovered that 17beta-estradiol (E2), and the two major phytoestrogens, genistein and quercetin, stimulate c-fos expression through ERalpha as well as through an ER-independent manner via the G protein-coupled receptor homologue GPR30.	Genistein	235-244	Fos proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	6-11	
11506505-10	2001	The results suggest that induction of apoptosis, G2 cell cycle arrest and inhibition of c-fos expression, AP-1 transactivation and ERK phosphorylation may contribute to the growth-inhibitory effect of genistein in some breast cell types, but none of these effects of genistein constitutes a generic mode of growth-arresting action.	Genistein	201-210	Fos proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	106-110	
11775869-7	2000	Curcumin (AP-1 inhibitor), staurosporine (PKC inhibitor), and genistein (PTK inhibitor) all reduced AP-1-mediated PAI-1 mRNA expression induced by thrombin in cultured MCs.	Genistein	62-71	Fos proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	100-104	
10771030-9	2000	Increased c-fos expression, but not CCK release, was suppressed by the MAP kinase (MEK) inhibitor PD98059, and by the tyrosine kinase inhibitor genistein.	Genistein	144-153	Fos proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	10-15	
9202212-3	1997	Using the tyrosine phosphorylation inhibitor, genistein, and electrophoretic mobility shift assay, we show that IL-6 and IFN-gamma induce nuclear factor STAT-3 and STAT-1 DNA-binding activity to the sis-inducible element of c-fos in a genistein-dependent pathway.	Genistein	235-244	Fos proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	224-229	
9849427-11	1998	Inhibition by genistein of EGF-induced c-fos mRNA transcription is probably related to its interruption of EGF receptor-linked protein tyrosine kinase, whereas genistein-induced growth arrest is not.	Genistein	14-23	Fos proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	39-44	
9849427-4	1998	Of the six agents, only genistein decreased EGF-induced, c-fos transcription (by 63% compared to control at 100 mumol/l).	Genistein	24-33	Fos proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	57-62	
9202212-7	1997	Furthermore, genistein treatment blocks the induction of c-fos and junB gene expression, demonstrating that tyrosine phosphorylation of STAT proteins is involved in the cytokine regulation of the Sertoli immediate early genes.	Genistein	13-22	Fos proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	57-62	
9177393-5	1997	The c-jun and c-fos mRNA stimulation elicited by TPA was reduced by the PKC inhibitors, chelerythrine and staurosporine, and could not be mimicked by 4alpha-phorbol 12,13-didecanoate (a phorbol ester that fails to activate PKC), whereas the stimulation induced by EGF was diminished by the PTK inhibitor, genistein.	Genistein	305-314	Fos proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	14-19