a proto-oncogenic receptor tyrosine kinase with high affinity for hepatocyte growth factor. The primary single chain precursor protein is post-translationally cleaved to produce the 45 kDa alpha- and 145 kDa beta-subunits, which are disulfide linked to form the mature receptor. Ligand-binding induces autophosphorylation at multiple tyrosines, which recruit several downstream signaling components, including Gab1, c-Cbl and PI3 kinase. Activating point mutations cause hereditary papillary renal carcinoma. Mutations also seen in sporadic renal cell carcinoma and childhood hepatocellular carcinoma. Upregulation in carcinomas and sarcomas correlates with metastasis and poor outcome. Some gastric carcinomas harbor a translocation that creates an activated TPR-Met fusion protein. A small molecule inhibitor (PHA-665752) shows an effect in gastric carcinoma xenografts. Inhibitors: SU11274, PHA-665752, mAbs. Two alternatively spliced human isoforms have been reported. Note: This description may include information from UniProtKB.
Protein type: Kinase, protein; Protein kinase, tyrosine (receptor); Protein kinase, TK; Membrane protein, integral; EC 188.8.131.52; TK group; Met family
Cellular Component: integral to plasma membrane; extracellular region; plasma membrane; integral to membrane; basal plasma membrane
Molecular Function: protein binding; protein-tyrosine kinase activity; protein phosphatase binding; hepatocyte growth factor receptor activity; ATP binding
Biological Process: axon guidance; skeletal muscle development; peptidyl-tyrosine phosphorylation; activation of MAPK activity; myoblast proliferation; protein amino acid autophosphorylation; muscle cell migration; myotube differentiation; glucose homeostasis; signal transduction; liver development; cell proliferation; cell surface receptor linked signal transduction; branching morphogenesis of a tube; adult behavior; positive regulation of transcription from RNA polymerase II promoter; brain development; placenta development
SS: The number of records in which this modification site was determined using site-specific methods. SS methods include amino acid sequencing, site-directed mutagenesis, modification site-specific antibodies, specific MS strategies, etc.