Mouse C-MET/HGFR ELISA Kit

Kit Components

 1. Recombinant Mouse C-MET standard: 2 vials

 2. One 96-well plate precoated with anti- Mouse C-MET Ab

 3. Sample diluent buffer: 12 mL - 1

 4. Detection antibody: 130 µL, dilution 1:100

 5. Streptavidin-HRP: 130 µL, dilution 1:100

 6. Antibody diluent buffer: 12 mL x1   

 7. Streptavidin-HRP diluent buffer: 12 mL x1

 8. TMB developing agent: 10 mL x1

9. Stop solution: 10 mL x1.

10. Washing solution (20x): 25 mL x1.

Background

HGF R (Hepatocyte growth factor receptor), also known as proto-oncogene c-Met (c-Met), is encoded by the MET gene in humans. Mature HGF R is a disulfide-linked dimer composed of a 50 kDa extracellular α chain and a 145 kDa transmembrane β chain. The extracellular domain (ECD) contains a seven bladed β propeller sema domain, a cysteine-rich PSI/MRS, and four Ig-like E-set domains, while the cytoplasmic region includes the tyrosine kinase domain. Proteolysis and alternative splicing generate additional forms of human HGF R with variable functional domains. The ECD of mouse HGF R shares 87% and 84% aa sequence identity with, human and rat HGF R. HGF R plays a central role in epithelial morphogenesis and cancer development. In the absence of ligand, HGF R forms non-covalent complexes with a variety of membrane proteins including CD44v6, CD151, EGF R, Fas, integrin α6/β4, Plexins B1, 2, 3, and MSP R/Ron. HGF stimulation induces HGF R downregulation via internalization and proteasome-dependent degradation. Ligation of one complex component triggers activation of the other, followed by cooperative signaling effects. Formation of some of these heteromeric complexes is a requirement for epithelial cell morphogenesis and tumor cell invasion. Genetic polymorphisms, chromosomal translocation, overexpression, and additional splicing and proteolytic cleavage of HGF R have been found in a wide range of cancers.