Recombinant mouse HGFR/c-MET protein

HGFR, also known as c-Met, is a receptor tyrosine kinase (RTK) that has been shown to be overexpressed and/or mutated in a variety of malignancies. It regulates many physiological processes including proliferation, scattering, morphogenesis and survival. This ligand binding at the cell surface induces autophosphorylation of MET on its intracellular domain that provides docking sites for downstream signaling molecules. This protein 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. Recombinant mouse HGF R/c-MET, fused to hIgG-His-tag at C-terminus, was expressed in insect cell and purified by using conventional chromatography techniques.