Overview:

c-MET is a receptor tyrosine kinase that binds hepatocyte growth factor (also known as scatter factor, HGF/SF). Stimulation by HGF causes c-MET to autophosphorylate at multiple tyrosines, including Y1234 and Y1235. Activated c-MET binds to various substrates, such as GAB1, GRB2, phosphatidylinositol 3-kinase (PI3K) and others. GAB1 is scaffold protein, which enables c-MET to elicit downstream signaling cascades, which include the well-characterized ERK/MAPK, PI3K–Akt/PKB, Crk–Rap and Rac–Pak pathways; leading to cell proliferation and cell survival.

References:

1. Birchmeier, C., et al.: Met, metastasis, motility and more. Nat. Rev. Mol. Cell Bio. 2003: 4; 915-925.

2. Fan, S., et al.: The multisubstrate adapter Gab1 regulates hepatocyte growth factor (scatter factor)-c-Met signaling for cell survival and DNA repair. Mol. Cell Biol. 2001: 21; 4968-84.

3. Longati, P., et al. Receptor tyrosine kinases as therapeutic targets: the model of the MET oncogene. Curr. Drug Targets. 2001: 2; 41-55.