Catalytic activity:ATP + a [protein]-L-tyrosine = ADP + a [protein]-L-tyrosine phosphate. ,Disease:Activation of MET after rearrangement with the TPR gene produces an oncogenic protein. ,Disease:Defects in MET are a cause of hepatocellular carcinoma (HCC) [MIM:114550]. ,Disease:Defects in MET are a cause of hereditary papillary renal carcinoma (HPRC) [MIM:605074]; also known as papillary renal cell carcinoma 2 (RCCP2) . HPRC is a form of inherited kidney cancer characterized by a predisposition to develop multiple , bilateral papillary renal tumors. The pattern of inheritance is consistent with autosomal dominant transmission with reduced penetrance. ,Disease:Defects in MET may be associated with gastric cancer. ,Disease:Genetic variations in MET may be associated with susceptibility to autism type 9 (AUTS9) [MIM:611015]. Autism is a neurodevelopmental disorder characterized by disturbance in language , perception and socialization. The disorder is classically defined by a triad of limited or absent verbal communication , a lack of reciprocal social interaction or responsiveness , and restricted , stereotypical , and ritualized patterns of interests and behavior. ,Domain:The kinase domain is involved in SPSB1 binding. ,Function:Receptor for hepatocyte growth factor and scatter factor. Has a tyrosine-protein kinase activity. Functions in cell proliferation , scattering , morphogenesis and survival. ,online information:C-MET entry ,similarity:Belongs to the protein kinase superfamily. Tyr protein kinase family. ,similarity:Contains 1 protein kinase domain. ,similarity:Contains 1 Sema domain. ,similarity:Contains 3 IPT/TIG domains. ,subunit:Heterodimer formed of an alpha chain (50 kDa) and a beta chain (145 kDa) which are disulfide linked. Binds PLXNB1 and GRB2. Interacts with SPSB1 , SPSB2 and SPSB4 (By similarity) . Interacts with INPP5D/SHIP1. When phosphorylated at Tyr-1356 , interacts with INPPL1/SHIP2. Interacts with RANBP9 and RANBP10 , as well as SPSB1 , SPSB2 , SPSB3 and SPSB4. SPSB1 binding occurs in the presence and in the absence of HGF , however HGF treatment has a positive effect on this interaction. Interacts with MUC20; prevents interaction with GRB2 and suppresses hepatocyte growth factor-induced cell proliferation. ,
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