PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 23778885-0 2013 Phosphorylation of cMet tyrosine residues in murine ascitic hepatic cancer cell lines with different lymph node metastatic potentials. Tyrosine 24-32 met proto-oncogene Mus musculus 19-23 26698536-3 2016 A structure-activity relationship (SAR) study of these substances led to identification of pyridazinone 19 as a highly selective and potent c-Met tyrosine inhibitor, which displays favorable pharmacokinetic properties in mice and significant antitumor activity against a c-Met driven EBC-1 tumor xenograft. Tyrosine 146-154 met proto-oncogene Mus musculus 140-145 23973484-5 2013 In search of functional signals related to 6PGD, we discovered that knockdown of 6PGD significantly inhibited phosphorylation of c-Met at tyrosine residues known to be critical for activity. Tyrosine 138-146 met proto-oncogene Mus musculus 129-134 23778885-4 2013 Following HGF treatment, the phosphorylation of cMet at Tyr 1313 and 1365 in Hca-F cells was higher, while the phosphorylation of cMet at Tyr 1349 was lower than that in Hca-P. Tyrosine 138-141 met proto-oncogene Mus musculus 130-134 23778885-6 2013 After FN treatment, the phosphorylation of cMet at Tyr 1313 and the activity of the PLCgamma/DAG/PKC signaling pathway was increased in Hca-F cells compared with Hca-P cells. Tyrosine 51-54 met proto-oncogene Mus musculus 43-47 23778885-7 2013 Following LN treatment, the phosphorylation of cMet at Tyr 1365 and the activity of PLCgamma/DAG/PKC was higher in Hca-F cells than in Hca-P cells. Tyrosine 55-58 met proto-oncogene Mus musculus 47-51 23778885-8 2013 Results of the current study indicate that a number of ligands stimulate the phosphorylation of cMet at various tyrosine residues, activating different signaling transduction pathways. Tyrosine 112-120 met proto-oncogene Mus musculus 96-100 23778885-9 2013 In addition, the same ligand was observed to phosphorylate different tyrosine residues on cMet in the two cell lines, as well as activate different intracellular signaling transduction pathways. Tyrosine 69-77 met proto-oncogene Mus musculus 90-94 23778885-10 2013 After cMet is activated, various tyrosine residues are phosphorylated, leading to the activation of the PI3K/AKT and PLCgamma/DAG/PKC signaling pathways to different extents in the two cells lines. Tyrosine 33-41 met proto-oncogene Mus musculus 6-10 23968914-6 2013 Ectopic expression of CD82 in Hepa1-6 cells inhibited HGF-stimulated tyrosine phosphorylation of cMet at Tyr1313 and Tyr1365 without affecting the expression of cMet. Tyrosine 69-77 met proto-oncogene Mus musculus 97-101 23749170-0 2013 Ganglioside GM3 promotes HGF-stimulated motility of murine hepatoma cell through enhanced phosphorylation of cMet at specific tyrosine sites and PI3K/Akt-mediated migration signaling. Tyrosine 126-134 met proto-oncogene Mus musculus 109-113 23749170-7 2013 All the observations indicate that ganglioside GM3 promotes HGF-stimulated motility of murine hepatoma cell through enhanced phosphorylation of cMet at specific tyrosine sites and PI3K/Akt-mediated migration signaling. Tyrosine 161-169 met proto-oncogene Mus musculus 144-148 23778885-3 2013 Cells were treated with HGF, fibronectin (FN) and laminin (LN), and the phosphorylated tyrosine residues of cMet and the activities of intracellular phospholipase Cgamma/diacylglycerol/protein kinase C (PLCgamma/DAG/PKC) and phosphoinositol-3-kinase/protein kinase B (PI3K/AKT) signaling pathways were analyzed comparatively in the two cell lines using western blot analysis and migration assays. Tyrosine 87-95 met proto-oncogene Mus musculus 108-112 23778885-4 2013 Following HGF treatment, the phosphorylation of cMet at Tyr 1313 and 1365 in Hca-F cells was higher, while the phosphorylation of cMet at Tyr 1349 was lower than that in Hca-P. Tyrosine 56-59 met proto-oncogene Mus musculus 48-52 21342325-8 2011 In these processes, c-Met tyrosine phosphorylation, which represented HGF signal activation, occurred in glomerular cells including podocytes. Tyrosine 26-34 met proto-oncogene Mus musculus 20-25 21342325-9 2011 When recombinant HGF was administrated to nephritic mice, c-Met tyrosine phosphorylation became evident in podocytes. Tyrosine 64-72 met proto-oncogene Mus musculus 58-63 19595710-0 2009 Disease-dependent reciprocal phosphorylation of serine and tyrosine residues of c-Met/HGF receptor contributes disease retardation of a transgenic mouse model of ALS. Tyrosine 59-67 met proto-oncogene Mus musculus 80-98 19595710-4 2009 Using double transgenic mice expressing HGF and mutated SOD1(G93A) (G93A/HGF), we showed that phosphorylation of c-Met tyrosine residues at positions 1230, 1234 and 1235 (phospho-Tyr), and thereby its activation, was slightly evident in G93A and highly obvious in G93A/HGF mice (but absent in WT and HGF-Tg mice). Tyrosine 119-127 met proto-oncogene Mus musculus 113-118 19595710-4 2009 Using double transgenic mice expressing HGF and mutated SOD1(G93A) (G93A/HGF), we showed that phosphorylation of c-Met tyrosine residues at positions 1230, 1234 and 1235 (phospho-Tyr), and thereby its activation, was slightly evident in G93A and highly obvious in G93A/HGF mice (but absent in WT and HGF-Tg mice). Tyrosine 179-182 met proto-oncogene Mus musculus 113-118 19595710-7 2009 Thus, c-Met activation is reciprocally regulated by phosphorylation between c-Met serine and tyrosine residues through PP2A induction in the presence or absence of mutant SOD1 expression, and HGF functions more efficiently in ALS and ALS-related diseases. Tyrosine 93-101 met proto-oncogene Mus musculus 6-11 8702829-4 1996 The loss of tyrosine phosphorylation of c-Met in suspension appears to depend, at least partly, on an increased cytosolic tyrosine phosphatase activity. Tyrosine 12-20 met proto-oncogene Mus musculus 40-45 17068118-6 2007 When c-Met tyrosine phosphorylation was blocked in the livers of BDL-treated mice by anti-HGF IgG, hepatic dysfunction became evident, associated with the acceleration of hepatocyte necrosis and apoptosis. Tyrosine 11-19 met proto-oncogene Mus musculus 5-10 17006939-2 2006 We have previously reported that beta-catenin forms a complex with c-Met (HGF receptor) that undergoes dissociation because of beta-catenin tyrosine phosphorylation on stimulation by HGF. Tyrosine 140-148 met proto-oncogene Mus musculus 67-72 17006939-2 2006 We have previously reported that beta-catenin forms a complex with c-Met (HGF receptor) that undergoes dissociation because of beta-catenin tyrosine phosphorylation on stimulation by HGF. Tyrosine 140-148 met proto-oncogene Mus musculus 74-86 11735009-6 2001 Phosphorylation of tyrosine residues in the c-Met beta chain also occurred in these stages. Tyrosine 19-27 met proto-oncogene Mus musculus 44-49 16476577-6 2006 When c-Met tyrosine phosphorylation was abolished by anti-HGF IgG, mucosal cell proliferation became faint, leading to delayed recovery from mucotitis, and vice versa in cases of HGF supplementation. Tyrosine 11-19 met proto-oncogene Mus musculus 5-10 15550554-5 2005 Treatment with HGF cDNA induced tyrosine phosphorylation of intestinal c-Met/HGF receptors, inhibited apoptosis, and promoted mitosis in intestinal epithelial cells, accelerating intestinal epithelial restoration and suppressing inflammation. Tyrosine 32-40 met proto-oncogene Mus musculus 71-76 15017381-7 2004 Likewise, intrahepatic invasion of cancer cells was inhibited by NK4 gene expression, and this anti-invasive effect was associated with in situ inhibition of c-Met receptor tyrosine phosphorylation. Tyrosine 173-181 met proto-oncogene Mus musculus 158-163 8822210-4 1996 HGF receptor/Met is expressed in SP1 cells and is constitutively tyrosine phosphorylated. Tyrosine 65-73 met proto-oncogene Mus musculus 0-12 1311683-11 1992 Furthermore, tyrosine phosphorylation of the c-met protein was stimulated by HGF treatment of Meth A cells, suggesting that it may be involved in the signal transduction of the growth inhibition of Meth A cells by HGF. Tyrosine 13-21 met proto-oncogene Mus musculus 45-50 8822210-6 1996 This finding suggests that constitutive tyrosine phosphorylation of HGF receptor/Met is sustained by an extracellular factor, most likely HGF. Tyrosine 40-48 met proto-oncogene Mus musculus 68-80 7515877-0 1994 Regulatory role of major tyrosine autophosphorylation site of kinase domain of c-Met receptor (scatter factor/hepatocyte growth factor receptor). Tyrosine 25-33 met proto-oncogene Mus musculus 79-84 7515877-2 1994 To assess the regulatory role of the major tyrosine autophosphorylation site (tyrosine 1233) of the mouse c-Met receptor in the tyrosine kinase activation of the receptor, we constructed a mutant receptor in which the tyrosine residue was replaced with phenylalanine. Tyrosine 43-51 met proto-oncogene Mus musculus 106-111 7515877-2 1994 To assess the regulatory role of the major tyrosine autophosphorylation site (tyrosine 1233) of the mouse c-Met receptor in the tyrosine kinase activation of the receptor, we constructed a mutant receptor in which the tyrosine residue was replaced with phenylalanine. Tyrosine 78-86 met proto-oncogene Mus musculus 106-111 7515877-2 1994 To assess the regulatory role of the major tyrosine autophosphorylation site (tyrosine 1233) of the mouse c-Met receptor in the tyrosine kinase activation of the receptor, we constructed a mutant receptor in which the tyrosine residue was replaced with phenylalanine. Tyrosine 78-86 met proto-oncogene Mus musculus 106-111 7514539-2 1994 In this paper, we report that the c-met protooncogene-transformed cells proliferate in a serum- and growth factor-free medium and exhibit constitutive tyrosine phosphorylation of several cellular proteins including the met protooncogene-encoded p145 and p185. Tyrosine 151-159 met proto-oncogene Mus musculus 34-39 7689722-2 1993 It was previously shown by cDNA transfection that the mitogenic effect of SF/HGF is mediated by activation of the tyrosine phosphorylation of the c-Met receptor (the c-met proto-oncogene product). Tyrosine 114-122 met proto-oncogene Mus musculus 146-151 7689722-2 1993 It was previously shown by cDNA transfection that the mitogenic effect of SF/HGF is mediated by activation of the tyrosine phosphorylation of the c-Met receptor (the c-met proto-oncogene product). Tyrosine 114-122 met proto-oncogene Mus musculus 166-171