PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 24719563-9 2014 ERK1/2 showed increased phosphorylation by genistein treatment after reperfusion, and an ERK1/2 inhibitor U0126 abolished this protective effect of genistein in terms of infarct volumes, neurological scores and cellular apoptosis. Genistein 43-52 mitogen-activated protein kinase 3 Mus musculus 0-6 28816409-7 2018 In vivo, genistein also reduced fasting glucose levels accompanied with reduced PEPCK-C expression and increased in AMPK and ERK1/2 phosphorylation states in the liver of genistein-treated alloxan-induced diabetic mice. Genistein 9-18 mitogen-activated protein kinase 3 Mus musculus 125-131 28816409-7 2018 In vivo, genistein also reduced fasting glucose levels accompanied with reduced PEPCK-C expression and increased in AMPK and ERK1/2 phosphorylation states in the liver of genistein-treated alloxan-induced diabetic mice. Genistein 171-180 mitogen-activated protein kinase 3 Mus musculus 125-131 24719563-9 2014 ERK1/2 showed increased phosphorylation by genistein treatment after reperfusion, and an ERK1/2 inhibitor U0126 abolished this protective effect of genistein in terms of infarct volumes, neurological scores and cellular apoptosis. Genistein 148-157 mitogen-activated protein kinase 3 Mus musculus 89-95 23829885-5 2014 However, treatment of MC3T3-E1 cells with 10 mum-genistein enhanced the phosphorylation of extracellular signal-regulated kinase 1/2, p38 mitogen-activated protein kinase (MAPK) and c-Jun N-terminal kinase 1/2 in a time-dependent manner. Genistein 49-58 mitogen-activated protein kinase 3 Mus musculus 91-132 16543731-10 2006 EGF also increased phosphorylation of p38 MAPK and p44/42 MAPKs, which was blocked by genistein or bisindolylmaleimide I, respectively. Genistein 86-95 mitogen-activated protein kinase 3 Mus musculus 51-54 20484465-6 2010 Pharmacological or molecular intervention of protein kinase A (PKA) or ERK1/2 completely abolished genistein-stimulated beta-cell proliferation, suggesting that both molecules are essential for genistein action. Genistein 99-108 mitogen-activated protein kinase 3 Mus musculus 71-77 20484465-10 2010 These results demonstrate that genistein may be a natural antidiabetic agent by directly modulating pancreatic beta-cell function via activation of the cAMP/PKA-dependent ERK1/2 signaling pathway. Genistein 31-40 mitogen-activated protein kinase 3 Mus musculus 171-177 18384126-5 2008 Genistein dose-dependently decreased the phosphorylation of ERK1/2 in mouse BMSC cultures. Genistein 0-9 mitogen-activated protein kinase 3 Mus musculus 60-66 18384126-8 2008 BMSC cultures treated with genistein in the presence of fibroblast growth factor-2 (FGF-2), an activator of the ERK1/2 signaling pathway, expressed normal levels of ERK1/2 activity, and, in so doing, are capable of undergoing adipogenesis. Genistein 27-36 mitogen-activated protein kinase 3 Mus musculus 112-118 18384126-8 2008 BMSC cultures treated with genistein in the presence of fibroblast growth factor-2 (FGF-2), an activator of the ERK1/2 signaling pathway, expressed normal levels of ERK1/2 activity, and, in so doing, are capable of undergoing adipogenesis. Genistein 27-36 mitogen-activated protein kinase 3 Mus musculus 165-171 15820502-12 2005 In addition, genistein, PKI, and bisindolylmaleimide I blocked the phosphorylation of p38 MAPK by insulin, suggesting a causal relationship. Genistein 13-22 mitogen-activated protein kinase 3 Mus musculus 90-94 12604671-7 2003 BK-induced ERK1/2 activation was Ca(2+)-calmodulin-independent but was sensitive to genistein, an inhibitor of tyrosine kinase(s). Genistein 84-93 mitogen-activated protein kinase 3 Mus musculus 11-17 15149738-6 2004 Genistein in the diet significantly down-regulated cell proliferation, EGFR, IGF-1R, ERK-1 and ERK-2, but not AR, ER-alpha, ER-beta, ErbB2, EGF, TGF-alpha, IGF-1, VEGF and VEGFR in prostates of TRAMP mice. Genistein 0-9 mitogen-activated protein kinase 3 Mus musculus 85-90 15149738-9 2004 Down-regulation of the tyrosine kinase regulated proteins, EGFR and IGF-1R, and of the downstream mitogen-activated protein kinases, ERK-1 and 2, with genistein in the diet provides a possible mechanism for prostate cancer chemoprevention. Genistein 151-160 mitogen-activated protein kinase 3 Mus musculus 133-144 9679653-8 1998 Genistein a PTK inhibitor inhibited the cisplatin induced expression of Ras and ERK-1. Genistein 0-9 mitogen-activated protein kinase 3 Mus musculus 80-85 11880592-11 2002 Genistein in the diet reduced the incidence of poorly differentiated prostatic adenocarcinomas in a dose-dependent manner and down-regulated androgen receptor, estrogen receptor-alpha, progesterone receptor, epidermal growth factor receptor, insulin-like growth factor-I, and extracellular signal-regulated kinase-1 but not estrogen receptor-beta and transforming growth factor-alpha mRNA expressions. Genistein 0-9 mitogen-activated protein kinase 3 Mus musculus 276-315 34514247-5 2021 The results revealed that genistein did not influence the behavior of ERalpha and ERbeta, whereas genistein immediately repressed the phosphorylation of ERK1/2. Genistein 98-107 mitogen-activated protein kinase 3 Mus musculus 153-159 33842915-0 2021 Genistein enhances expression of extracellular regulated kinases (ERK) 1/2, and learning and memory of mouse. Genistein 0-9 mitogen-activated protein kinase 3 Mus musculus 33-74