MET Gene (Protein Coding)

• This gene encodes a member of the receptor tyrosine kinase family of proteins and the product of the proto-oncogene MET. The encoded preproprotein is proteolytically processed to generate alpha and beta subunits that are linked via disulfide bonds to form the mature receptor. Further processing of the beta subunit results in the formation of the M10 peptide, which has been shown to reduce lung fibrosis. Binding of its ligand, hepatocyte growth factor, induces dimerization and activation of the receptor, which plays a role in cellular survival, embryogenesis, and cellular migration and invasion. Mutations in this gene are associated with papillary renal cell carcinoma, hepatocellular carcinoma, and various head and neck cancers. Amplification and overexpression of this gene are also associated with multiple human cancers. [provided by RefSeq, May 2016]

• Mesenchymal Epithelial Transition MET is a prototypical receptor tyrosine kinase. Its ligand is Hepatocyte Growth Factor (HGF). MET alterations are drivers of human cancer. Amplification and resulting overexpression has been reported in several cancers, and make the receptor's activity independent of HGF. Gene fusions also decouple kinase activity from the cell membrane and render it constitutively active. Finally, exclusion of the juxtamembrane (JM) domain of the kinase by "skipping" of exon 14 activates the kinase.

MET (MET Proto-Oncogene, Receptor Tyrosine Kinase) is a Protein Coding gene. Diseases associated with MET include Renal Cell Carcinoma, Papillary, 1 and Deafness, Autosomal Recessive 97. Among its related pathways are PI3K/AKT activation and RET signaling. Gene Ontology (GO) annotations related to this gene include transferase activity, transferring phosphorus-containing groups and protein tyrosine kinase activity. An important paralog of this gene is MST1R.

• Receptor tyrosine kinase that transduces signals from the extracellular matrix into the cytoplasm by binding to hepatocyte growth factor/HGF ligand. Regulates many physiological processes including proliferation, scattering, morphogenesis and survival. Ligand binding at the cell surface induces autophosphorylation of MET on its intracellular domain that provides docking sites for downstream signaling molecules. Following activation by ligand, interacts with the PI3-kinase subunit PIK3R1, PLCG1, SRC, GRB2, STAT3 or the adapter GAB1. Recruitment of these downstream effectors by MET leads to the activation of several signaling cascades including the RAS-ERK, PI3 kinase-AKT, or PLCgamma-PKC. The RAS-ERK activation is associated with the morphogenetic effects while PI3K/AKT coordinates prosurvival effects. During embryonic development, MET signaling plays a role in gastrulation, development and migration of muscles and neuronal precursors, angiogenesis and kidney formation. In adults, participates in wound healing as well as organ regeneration and tissue remodeling. Promotes also differentiation and proliferation of hematopoietic cells. May regulate cortical bone osteogenesis (By similarity).

  • MET_HUMAN,P08581
• (Microbial infection) Acts as a receptor for Listeria monocytogenes internalin InlB, mediating entry of the pathogen into cells.

  • MET_HUMAN,P08581

• The MET receptor, also known as hepatocyte growth factor receptor (HGFR), is a proto-oncogenic receptor tyrosine kinase. The endogenous ligand for MET is hepatocyte growth factor/scatter factor (HGF), a disulfide-linked heterodimeric molecule.

• HGNC(7029)
• Entrez Gene(4233)
• Ensembl(ENSG00000105976)
• OMIM(164860)
• UniProtKB(P08581)
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• Monarch Initiative
• Search for MET at DataMed
• Search for MET at HumanCyc

No data available for PharmGKB "VIP" Summary , Rfam classification and piRNA Summary for MET Gene

No data available for Transcription Factor Targets and HOMER Transcription for MET Gene

Subcellular locations from UniProtKB/Swiss-Prot for MET Gene