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• W2023442980 abstract "The HGF receptor family includes tyrosine kinases encoded by three oncogenes: MET, Sea and RON. The ability to promote uncontrolled proliferation represents only one of the two facets of their oncogenic potential. The three members of the HGF receptor family share a unique functional feature: they mediate cell motility in physiological conditions, and invasiveness in their activated versions. This suggests a role in tumorigenesis and in progression to the metastatic phenotype. The p190MET receptor is a heterodimer of two (α β) disulfide-linked protein subunits. Two receptor isoforms, carrying a native ligand binding domain but lacking the kinase domain, arise from alternative post-transcriptional processing. In physiological conditions, HGF binding triggers tyrosine autophosphorylation of its receptor, upregulating its kinase activity: site-directed mutagenesis of two tyrosine residues involved in the positive regulation of the catalytic activity (y1234 or y1235) strongly impairs the transforming potential of the oncogenic counterpart of the receptor. Negative regulation of the kinase activity occurs through distinct pathways involving protein kinase C or increase in the intracellular Ca2+ concentration. Receptor autophosphorylation of a multifunctional docking site, made of the duplicated degenerate sequence YVH/NV, mediates interactions with multiple SH2containing signalling molecules, including PI 3-kinase, phospholipaseC-γ, pp60c – Src, and the GRB-2/SoS complex. Mutation of the two tyrosines (y1349 and y1356) of the bidentate docking site results in the abrogation of the transforming activity in the oncogenic counterpart of the receptor. The MET oncogene is overexpressed (activated) in a significant fraction of human cancers, including thyroid and colorectal carcinomas. MET amplification is found in metastases. Cells transfected with the MET proto-oncogene display a motile and invasive phenotype in the presence of HGF. Recently we have identified the ligand for another member of the MET family, the RON receptor. We have shown that Ron is activated upon binding MSP (Macrophage Activating Protein), an HGF-like polypeptide involved in cell proliferation and chemotaxis. The HGF receptor family includes tyrosine kinases encoded by three oncogenes: MET, Sea and RON. The ability to promote uncontrolled proliferation represents only one of the two facets of their oncogenic potential. The three members of the HGF receptor family share a unique functional feature: they mediate cell motility in physiological conditions, and invasiveness in their activated versions. This suggests a role in tumorigenesis and in progression to the metastatic phenotype. The p190MET receptor is a heterodimer of two (α β) disulfide-linked protein subunits. Two receptor isoforms, carrying a native ligand binding domain but lacking the kinase domain, arise from alternative post-transcriptional processing. In physiological conditions, HGF binding triggers tyrosine autophosphorylation of its receptor, upregulating its kinase activity: site-directed mutagenesis of two tyrosine residues involved in the positive regulation of the catalytic activity (y1234 or y1235) strongly impairs the transforming potential of the oncogenic counterpart of the receptor. Negative regulation of the kinase activity occurs through distinct pathways involving protein kinase C or increase in the intracellular Ca2+ concentration. Receptor autophosphorylation of a multifunctional docking site, made of the duplicated degenerate sequence YVH/NV, mediates interactions with multiple SH2containing signalling molecules, including PI 3-kinase, phospholipaseC-γ, pp60c – Src, and the GRB-2/SoS complex. Mutation of the two tyrosines (y1349 and y1356) of the bidentate docking site results in the abrogation of the transforming activity in the oncogenic counterpart of the receptor. The MET oncogene is overexpressed (activated) in a significant fraction of human cancers, including thyroid and colorectal carcinomas. MET amplification is found in metastases. Cells transfected with the MET proto-oncogene display a motile and invasive phenotype in the presence of HGF. Recently we have identified the ligand for another member of the MET family, the RON receptor. We have shown that Ron is activated upon binding MSP (Macrophage Activating Protein), an HGF-like polypeptide involved in cell proliferation and chemotaxis." @default.
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• W2023442980 date "1995-11-01" @default.
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• W2023442980 title "1010 Control of invasive cell growth by receptors of the HGF family" @default.
• W2023442980 doi "https://doi.org/10.1016/0959-8049(95)96258-f" @default.
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