This purified ABfinity™ recombinant rabbit monoclonal antibody is specific to human c-Met and based on sequence identity reactivity with primates is expected. C-Met (hepatocyte growth factor receptor), is also known as HGFR, AUTS9, and RCCP2. ABfinity™ recombinant rabbit anti-c-Met monoclonal antibody is used in western blotting, ELISA, immunocytochemistry, and immunofluorescence applications.
• Applications: Validated applications for this rabbit anti-c-Met monoclonal antibody are western blotting, ELISA, and immunofluorescence.
• Host Species and Isotype: The host species and isotype of the antibody is rabbit IgG.
• Clone ID of Monoclonal Antibody (mAb): The rabbit anti-c-Met monoclonal antibody clone is 22H22L13.
• Reactivity: Reacts with human c-Met.
• Product Size: Rabbit anti-c-Met monoclonal antibody is available in a 100 µg size.
The c-Met protein is a receptor tyrosine kinase encoded by the c-Met proto-oncogene. c-Met, also known as HGF receptor or SF receptor, is activated by hepatocyte growth factor (HGF) or scatter factor (SF), and is composed of alpha and beta subunits linked by disulfide bonds. The alpha subunit of c-Met is extracellular and heavily glycosylated; the beta subunit contains an extracellular portion involved in ligand binding, a transmembrane segment, and a cytoplasmic tyrosine kinase domain. The truncated cytoplasmic region of c-Met has constitutive kinase activity and is oncogenic, but requires the first 39 amino acids of the juxtamembrane domain and the regulatory tyrosine in the catalytic domain to enact its transforming potential.
Activation of c-Met signaling has been implicated in tumor cell angiogenesis, proliferation, enhanced cell motility, and metastasis. Phosphorylation of key adhesion proteins, including paxillin, focal adhesion kinase, and PYK2, has been observed in response to c-Met stimulation in lung cancer cells. In the highly metastatic KM12SM colorectal carcinoma cell line, activation of c-Met leads to increased survival and growth under anchorage-independent conditions, increased cell migration, and elevated levels of Tcf target genes. Dysregulated c-Met expression has been detected at both protein and mRNA levels in a variety of human carcinomas and sarcomas. Up to a 2.5-fold increase in mRNA expression has been reported in colorectal tumor tissues, and upregulation of the c-Met protein in association with increasingly malignant behavior has been described in prostate cancer, cutaneous malignant melanoma, and breast cancer.
Two recent studies using clone 3D4 for immunohistochemistry in lymph node-negative breast carcinoma tissues demonstrated that high levels of c-Met expression is associated with poor patient clinical outcome with 20–40 years of follow-up. Further, antibodies against the intracellular but not the extracellular domain of c-Met were prognostic, suggesting that overexpression of the cytoplasmic tail of c-Met may play an important role in breast cancer progression.