PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 8218364-9 1993 Tyrosine kinase inhibitors (erbstatin and genistein) inhibited O2- release induced by FMLP, but not by PMA. Genistein 42-51 formyl peptide receptor 1 Homo sapiens 86-90 8804796-5 1996 Superoxide production augmented by FLRX was diminished by the addition of staurosporine and H-7, when PMNs were stimulated with PMA, and by the addition of genistein, when PMNs were stimulated with fMLP. Genistein 156-165 formyl peptide receptor 1 Homo sapiens 198-202 1372506-1 1992 Superoxide production by human neutrophils stimulated with FMLP and soluble aggregated human IgG were inhibited in a dose dependent manner by two kinds of tyrosine kinase inhibitors, erbstatin and genistein. Genistein 197-206 formyl peptide receptor 1 Homo sapiens 59-63 8219237-7 1993 By contrast, the tyrosine kinase inhibitor genistein (2 to 80 mumol/L) depressed fMLP-induced RB whatever the duration of PMN treatment. Genistein 43-52 formyl peptide receptor 1 Homo sapiens 81-85 1312809-4 1992 The oxygen burst induced by FMLP or OZ was inhibited by genistein and alpha-cyano-3-ethoxy-4-hydroxy-5-phenylthiomethylcinnamamid (ST638), which are inhibitors of tyrosine kinase (TK), and was enhanced by 1-(5-isoquinoline-sulfonyl)-3-methyl-piperazine (H-7) and staurosporine, which are inhibitors of protein kinase C (PKC). Genistein 56-65 formyl peptide receptor 1 Homo sapiens 28-32 1312809-7 1992 Furthermore, O.-2 generation by guinea pig peritoneal neutrophils, which are already primed in vivo, was induced markedly by FMLP by a mechanism which was stimulated by a low concentration of genistein or ST638. Genistein 192-201 formyl peptide receptor 1 Homo sapiens 125-129 7679431-11 1993 Treatment with genistein, a tyrosine kinase inhibitor, reduced the tyrosine phosphorylation of the 40- and 42-kDa proteins in a dose-dependent manner, decreased the activation of the MAP kinases, and inhibited the production of superoxide anion by FMLP-stimulated neutrophils. Genistein 15-24 formyl peptide receptor 1 Homo sapiens 248-252 17845735-8 2008 PMN homotypic aggregates, stimulated by fMLP, were significantly reduced (24 (sem 12) and 51 (sem 14) % of control) by 100 microm genistein and equol. Genistein 130-139 formyl peptide receptor 1 Homo sapiens 40-44 19218646-10 2008 In a Ca(2+)-free medium, a strong relationship between intracellular Ca(2+) and the response to fMLP after incubation with tyrphostin was found (P<0.001) The genistein did not influence the intracellular Ca(2+) in non-stimulated cells. Genistein 161-170 formyl peptide receptor 1 Homo sapiens 96-100 15753257-7 2005 In addition, genistein, a tyrosine kinase inhibitor, and SB203580, a p38 mitogen-activated protein kinase (p38MAPK) inhibitor, completely reversed the decreased level of fMLP binding and increased the level of CD11b expression after IL-18 treatment. Genistein 13-22 formyl peptide receptor 1 Homo sapiens 170-174 12521225-6 2002 The superoxide generation induced by fMLP in the DCEG-treated cells was suppressed by genistein. Genistein 86-95 formyl peptide receptor 1 Homo sapiens 37-41 15229106-7 2004 Wortmannin, a phosphatidylinositol 3-kinase (PI3K) kinase inhibitor, and genistein, a nonspecific tyrosine kinase inhibitor, strongly inhibited fMLP-induced elastase release both in the presence and in the absence of fibrinogen. Genistein 73-82 formyl peptide receptor 1 Homo sapiens 144-148 10666044-3 2000 Treatment with genistein (10(-4) M) and PGE(2) (10(-6) M) resulted in synergistic elevations in R and additive reductions in mucosal-to-serosal fluxes of [(3)H]FMLP and [(3)H]mannitol, whereas treatment with genistein alone had no effect. Genistein 15-24 formyl peptide receptor 1 Homo sapiens 160-164 11944907-4 2002 Genistein inhibited PLD activity with an IC(50) value of 12.2 microM in fMLP- and 107 microM in phorbol myristate acetate (PMA)-stimulated cells. Genistein 0-9 formyl peptide receptor 1 Homo sapiens 72-76 11944907-7 2002 These results demonstrate differential regulation of PLD activity and degranulation of primary granules by genistein and EGCG in fMLP-stimulated neutrophils. Genistein 107-116 formyl peptide receptor 1 Homo sapiens 129-133 10049498-6 1999 Genistein suppressed the fMLP-induced superoxide generation in the L-CK-treated cells more efficiently than that in the D-CK-treated cells. Genistein 0-9 formyl peptide receptor 1 Homo sapiens 25-29 10614786-4 1999 Three tyrosine kinases inhibitors, ST-638, methyl 2,5-dihydroxycinnamate, and genistein reduced fMLP-stimulated PLD activity by up to 80%. Genistein 78-87 formyl peptide receptor 1 Homo sapiens 96-100 10619578-7 1999 Genistein and bisindolylmaleimide significantly inhibited the fMLP-induced ROS in all groups. Genistein 0-9 formyl peptide receptor 1 Homo sapiens 62-66 10408834-7 1999 Both the FMLP- and the TNF-alpha-dependent systems were also found to be equally susceptible to inhibition by various inhibitors of kinases (genistein, staurosporin, 1-(5-isoquinolinnylsulphonyl)-2-methylpiperazine and wortmannin). Genistein 141-150 formyl peptide receptor 1 Homo sapiens 9-13 10048787-10 1999 However, responses to fMLP and IFN-gamma were both depressed by pertussis toxin, and the IFN-gamma responses were, in addition, inhibited by the tyrosine kinase inhibitor genistein. Genistein 171-180 formyl peptide receptor 1 Homo sapiens 22-26 10191961-1 1999 The tyrosine kinase inhibitor genistein (5-200 microM) suppressed Ca(2+)-dependent fMLP (1 microM) and ATP (100 microM)-induced release of the lysosomal enzyme, beta-glucuronidase from neutrophil-like HL-60 granulocytes. Genistein 30-39 formyl peptide receptor 1 Homo sapiens 83-87 10191961-3 1999 Genistein (200 microM) suppressed fMLP (1 microM) and ATP (100 microM)-induced Ca2+ mobilization, by 30-40%. Genistein 0-9 formyl peptide receptor 1 Homo sapiens 34-38 10191961-6 1999 In the absence of extracellular Ca2+, genistein had a small additional inhibitory effect on fMLP and ATP-induced beta-glucuronidase release, suggesting an additional inhibitory site of action. Genistein 38-47 formyl peptide receptor 1 Homo sapiens 92-96 9586797-4 1998 Herbimycin A and genistein decreased the fMLP- and OZ-induced superoxide generations after priming by Pro-Pro. Genistein 17-26 formyl peptide receptor 1 Homo sapiens 41-45 9642137-6 1998 The superoxide generation induced by PMA with CS-I was suppressed by H-7 and was enhanced by genistein, while that by fMLP with CS-II was suppressed by genistein and was enhanced by H-7. Genistein 152-161 formyl peptide receptor 1 Homo sapiens 118-122 9256158-6 1997 Pretreatment with genistein, an inhibitor of PTKs, significantly inhibited O2- production in both Aroclor 1242- and fMLP-treated neutrophils; however, daidzein, a structural analogue of genistein which lacks activity against PTKs, was without effect. Genistein 18-27 formyl peptide receptor 1 Homo sapiens 116-120 9427721-6 1998 The protein kinase C (PKC) inhibitor, calphostin C, and the tyrosine kinase inhibitor, genistein, inhibited both PMA- and fMLP-stimulated 2-DOG uptake. Genistein 87-96 formyl peptide receptor 1 Homo sapiens 122-126 9427721-7 1998 In contrast, genistein inhibited fMLP-induced superoxide production, but had little effect on the PMA-induced response, while staurosporine differentially inhibited PMA-induced superoxide production. Genistein 13-22 formyl peptide receptor 1 Homo sapiens 33-37 9167937-4 1997 The inhibition of tyrosine kinases by genistein (1-25 micrograms/ml) completely abolished H2O2 release by fMLP-activated neutrophils; conversely, .NO production increased about 1.5- and 3-fold with fMLP and PMA, respectively. Genistein 38-47 formyl peptide receptor 1 Homo sapiens 106-110 9167937-4 1997 The inhibition of tyrosine kinases by genistein (1-25 micrograms/ml) completely abolished H2O2 release by fMLP-activated neutrophils; conversely, .NO production increased about 1.5- and 3-fold with fMLP and PMA, respectively. Genistein 38-47 formyl peptide receptor 1 Homo sapiens 198-202