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Mouse c-MET / HGFR Protein (Fc Tag)

AI838057,c-Met,HGF,HGFR,Par4

Catalog Number P50622-M02H
Organism Species Mouse
Host Human Cells
Synonyms AI838057,c-Met,HGF,HGFR,Par4
Molecular Weight The recombinant mouse Met/Fc chimera is a disulfide-linked homodimer of the Met which is a heterodimer composed of the proteolytically cleaved α and β subunits. Each α and β together with the C-terminal Fc tag consists of 1146 amino acids and has a predicted molecular mass of 128 (α =32 + Fc tagged β=96) kDa. The apparent molecular mass of the rm MET/Fc heterodimer thus is approximately 43 kDa and 115-120 kDa respectively in SDS-PAGE under reducing conditions due to glycosylation.
predicted N Glu 25 & Ser 307
SDS-PAGE
Purity > 92 % as determined by SDS-PAGE
Protein Construction A DNA sequence encoding the mouse MET (NP_032617.2) extracellular domain (Met 1-Asn 929) was fused with the Fc region of human IgG1 at the C-terminus.
Bio-activity Measured by its binding ability in a functional ELISA . Immobilized human HGF at 2 μg/ml (100 μl/well) can bind mouse HGFR with a linear ranger of 1.28-32ng/ml.
Research Area Cancer |Signal transduction |Protein Phosphorylation |Tyrosine Kinase |Receptor Tyrosine Kinases
Formulation Lyophilized from sterile PBS, pH 7.4
1. Normally 5 % - 8 % trehalose and mannitol are added as protectants before lyophilization. Specific concentrations are included in the hardcopy of COA.
Background Hepatocyte growth factor receptor (HGFR), also known as c-Met or mesenchymal-epithelial transition factor (MET), is a receptor tyrosine kinase (RTK) that has been shown to be overexpressed and/or mutated in a variety of malignancies. HGFR protein is produced as a single-chain precursor, and HGF is the only known ligand. Normal HGF/HGFR signaling is essential for embryonic development, tissue repair or wound healing, whereas aberrantly active HGFR has been strongly implicated in tumorigenesis, particularly in the development of invasive and metastatic phenotypes. HGFR protein is a multifaceted regulator of growth, motility, and invasion, and is normally expressed by cells of epithelial origin. Preclinical studies suggest that targeting aberrant HGFR signaling could be an attractive therapy in cancer.
Reference
  • McGill GG, et al. (2006) c-Met expression is regulated by Mitf in the melanocyte lineage. J Biol Chem. 281(15): 10365-73.
  • Garcia S, et al. (2007) c-Met overexpression in inflammatory breast carcinomas: automated quantification on tissue microarrays. British journal of cancer. 96(2): 329-35.
  • Socoteanu MP, et al. (2008) c-Met targeted therapy of cholangiocarcinoma. World J Gastroenterol. 14(19): 2990-4.
  • Kong DS, et al. (2009) Prognostic significance of c-Met expression in glioblastomas. Cancer. 115(1): 140-8.