PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 28659710-10 2017 alphavbeta5 integrin inhibition via genistein, an anti-alphavbeta5 antibody, or beta5 siRNA knockdown abrogated the FGF-2-induced increase in cell-associated vitronectin and increased plasminogen system activity. Genistein 36-45 fibroblast growth factor 2 Homo sapiens 116-121 19711039-6 2009 This bFGF-induced [Mg(2+)](i) increase was blocked by tyrosine kinase inhibitors (tyrphostin A-23 and genistein), phosphatidylinositol 3-kinase (PI3K) inhibitors (wortmannin and LY294002) and a phospholipase Cgamma (PLCgamma) inhibitor (U73122). Genistein 102-111 fibroblast growth factor 2 Homo sapiens 5-9 19119629-7 2008 bFGF significantly elevated the intracellular free Ca2+ concentration, however its stimulating effect was remarkably alleviated when the fibroblasts were pre-treated by Genistein. Genistein 169-178 fibroblast growth factor 2 Homo sapiens 0-4 18785412-10 2008 Under the condition of pretreatment with genistein, the activities of TPK and signal pathway protein expressions in HSFb showed a downward trend after stimulation with bFGF. Genistein 41-50 fibroblast growth factor 2 Homo sapiens 168-172 17706452-7 2008 The specific tyrosine kinase inhibitor, genistein completely blocked the effects of FGF-2 and glycosaminoglycans on melanoma proliferation whereas the use of the neutralizing antibody for FGF-2 showed that the mitogenic effect of chondroitin sulfate involves the interaction of FGF-2 with its receptors. Genistein 40-49 fibroblast growth factor 2 Homo sapiens 84-89 16722796-0 2006 Inhibitive effect of genistein on hypoxia-induced basic fibroblast growth factor expression in human retinal pigment epithelium cells. Genistein 21-30 fibroblast growth factor 2 Homo sapiens 50-80 16722796-1 2006 AIM: The time course changes of basic fibroblast growth factor (bFGF) expression induced by hypoxia and the effects of genistein on hypoxia-induced bFGF expression in the human retinal pigment epithelium (RPE) cells were studied. Genistein 119-128 fibroblast growth factor 2 Homo sapiens 148-152 16722796-6 2006 With pretreatment of genistein (10, 20, 50, 100, and 200 microM) for 30 min, the elevated expression of bFGF mRNA was suppressed in a concentration-dependent manner. Genistein 21-30 fibroblast growth factor 2 Homo sapiens 104-108 16722796-7 2006 bFGF mRNA expression was reduced to 30.4% by 200 microM of genistein when compared with that untreated with genistein. Genistein 59-68 fibroblast growth factor 2 Homo sapiens 0-4 16722796-7 2006 bFGF mRNA expression was reduced to 30.4% by 200 microM of genistein when compared with that untreated with genistein. Genistein 108-117 fibroblast growth factor 2 Homo sapiens 0-4 16722796-10 2006 Genistein (10, 20, 50, 100, and 200 microM) could also suppress bFGF protein expression in a concentration-dependent manner. Genistein 0-9 fibroblast growth factor 2 Homo sapiens 64-68 16722796-12 2006 CONCLUSIONS: These results suggested that suppression of bFGF expression in RPE cells might partly account for the inhibitive effect of genistein on retinal neovascularization in vivo. Genistein 136-145 fibroblast growth factor 2 Homo sapiens 57-61 15733437-9 2004 Genistein at 0.5 mmol/L significantly inhibited bFGF induced changes of calcium. Genistein 0-9 fibroblast growth factor 2 Homo sapiens 48-52 15653093-5 2004 When genistein was supplemented to the bath solution, a significant activation of BK(Ca) by bFGF was observed during a time interval of 6-20 min (n=17, p<0.01). Genistein 5-14 fibroblast growth factor 2 Homo sapiens 92-96 12761886-10 2003 In conclusion, these data suggest that genistein, apigenin, and 3-hydroxyflavone inhibit in vitro angiogenesis, in part via preventing VEGF/bFGF-induced MMP-1 and uPA expression and the activation of pro-MMP-2, and via modulating their inhibitors, TIMP-1 and -2, and PAI-1. Genistein 39-48 fibroblast growth factor 2 Homo sapiens 140-144 11399257-8 2001 The all-trans-RA- and bFGF-mediated increases in PAI-1 mRNA levels were markedly attenuated by the tyrosine kinase inhibitor genistein, but not by MEK1 or p38MAP kinase inhibitors. Genistein 125-134 fibroblast growth factor 2 Homo sapiens 22-26 10866818-8 2000 The tyrosine kinase inhibitor genistein caused a dose-dependent inhibition of TIMP-1 protein induction by ATRA and bFGF. Genistein 30-39 fibroblast growth factor 2 Homo sapiens 115-119 9808840-7 1998 RESULTS: The fibroblastic morphology induced by FGF-2 reverted to a polygonal shape in cells treated with anti-FGF-2 antibody, anti-phosphatidylinositol 3-kinase antibody, LY294002, and genistein, while anti-phospholipase C gamma1 antibody did not to reverse the modulated cell morphology. Genistein 186-195 fibroblast growth factor 2 Homo sapiens 48-53 9808840-7 1998 RESULTS: The fibroblastic morphology induced by FGF-2 reverted to a polygonal shape in cells treated with anti-FGF-2 antibody, anti-phosphatidylinositol 3-kinase antibody, LY294002, and genistein, while anti-phospholipase C gamma1 antibody did not to reverse the modulated cell morphology. Genistein 186-195 fibroblast growth factor 2 Homo sapiens 111-116 9808840-8 1998 Cell proliferation mediated by FGF-2 was blocked by metabolic inhibitors (genistein, LY294002 and wortmannin); genistein inhibited FGF-mediated cell proliferation in a dose-response manner and had a maximum inhibition of 80% at 100 microM, while inhibitors of phosphatidylinositol 3-kinase had less inhibitory effect than did genistein. Genistein 74-83 fibroblast growth factor 2 Homo sapiens 31-36 9808840-8 1998 Cell proliferation mediated by FGF-2 was blocked by metabolic inhibitors (genistein, LY294002 and wortmannin); genistein inhibited FGF-mediated cell proliferation in a dose-response manner and had a maximum inhibition of 80% at 100 microM, while inhibitors of phosphatidylinositol 3-kinase had less inhibitory effect than did genistein. Genistein 74-83 fibroblast growth factor 2 Homo sapiens 31-34 9808840-8 1998 Cell proliferation mediated by FGF-2 was blocked by metabolic inhibitors (genistein, LY294002 and wortmannin); genistein inhibited FGF-mediated cell proliferation in a dose-response manner and had a maximum inhibition of 80% at 100 microM, while inhibitors of phosphatidylinositol 3-kinase had less inhibitory effect than did genistein. Genistein 111-120 fibroblast growth factor 2 Homo sapiens 31-34 9808840-8 1998 Cell proliferation mediated by FGF-2 was blocked by metabolic inhibitors (genistein, LY294002 and wortmannin); genistein inhibited FGF-mediated cell proliferation in a dose-response manner and had a maximum inhibition of 80% at 100 microM, while inhibitors of phosphatidylinositol 3-kinase had less inhibitory effect than did genistein. Genistein 111-120 fibroblast growth factor 2 Homo sapiens 31-34 7763235-5 1995 b-FGF-induced synovial cell growth was inhibited by protein tyrosine kinase (PTK) inhibitors, herbimycin A and genistein, but not by H7 that inhibits protein kinase C (PKC). Genistein 111-120 fibroblast growth factor 2 Homo sapiens 0-5 8304417-3 1994 bFGF-stimulated PLD activity was inhibited by genistein (5 microM; P < 0.02) and the PKC inhibitor 1-(5-isoquinolinylsulfonyl)-2-methylpiperazine (H-7, 5 microM; P < 0.001) as well as by the removal of calcium from extracellular environment. Genistein 46-55 fibroblast growth factor 2 Homo sapiens 0-4 8304491-2 1994 Two tyrosine kinase inhibitors, genistein and methyl 2,5-dihydroxycinnamate, showed reversible, dose-dependent inhibition of bFGF-stimulated DNA synthesis in CVEC with half-maximal inhibitory concentrations of 12 and 3 microM, respectively. Genistein 32-41 fibroblast growth factor 2 Homo sapiens 125-129