Anti-Met (c-Met) Antibody Picoband® Fluoro647 Conjugated

C-Met, also called MET and hepatocyte growth factor receptor (HGFR), is a protein that in humans is encoded by the MET gene. It is mapped to 7q31.2. The protein possesses tyrosine kinase activity. MET is a membrane receptor that is essential for embryonic development and wound healing. It induces several biological responses that collectively give rise to a program known as invasive growth. MET is deregulated in many types of human malignancies, including cancers of kidney, liver, stomach, breast, and brain. Normally, only stem cells and progenitor cells express MET, which allows these cells to grow invasively in order to generate new tissues in an embryo or regenerate damaged tissues in an adult. However, cancer stem cells are thought to hijack the ability of normal stem cells to express MET, and thus become the cause of cancer persistence and spread to other sites in the body.

Hepatocyte growth factor receptor; HGF receptor;2.7.10.1; HGF/SF receptor; Proto-oncogene c-Met; Scatter factor receptor; SF receptor; Tyrosine-protein kinase Met; MET

E.coli-derived human Met recombinant protein (Position: D208-S407) . Human Met shares 90% and 91% amino acid (aa) sequences identity with mouse and rat Met, respectively.

Expressed in normal hepatocytes as well as in epithelial cells lining the stomach, the small and the large intestine. Found also in basal keratinocytes of esophagus and skin. High levels are found in liver, gastrointestinal tract, thyroid and kidney. Also present in the brain. .

Cancer, Cancer Susceptibility, Epigenetics and Nuclear Signaling, Oncoproteins, Oncoproteins/Suppressors, Protein Phosphorylation, Proto-Oncogenes, Receptor Tyrosine Kinases, Signal Transduction, Transcription, Tyrosine Kinases

Receptor tyrosine kinase that transduces signals from the extracellular matrix into the cytoplasm by binding to hepatocyte growth factor/HGF ligand. Regulates many physiological processes including proliferation, scattering, morphogenesis and survival. Ligand binding at the cell surface induces autophosphorylation of MET on its intracellular domain that provides docking sites for downstream signaling molecules. Following activation by ligand, 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. During embryonic development, MET signaling plays a role in gastrulation, development and migration of muscles and neuronal precursors, angiogenesis and kidney formation. In adults, participates in wound healing as well as organ regeneration and tissue remodeling. Promotes also differentiation and proliferation of hematopoietic cells.

1. Bottaro DP, Rubin JS, Faletto DL, Chan AM, Kmiecik TE, Vande Woude GF, Aaronson SA (February 1991) . Identification of the hepatocyte growth factor receptor as the met proto-oncogene product. Science 251 (4995) : 802–4. 2. Galland F, Stefanova M, Lafage M, Birnbaum D (1992) . Localization of the 5' end of the MCF2 oncogene to human chromosome 15q15----q23. Cytogenet. Cell Genet. 60 (2) : 114–6. 3. Cooper CS (January 1992) . The met oncogene: from detection by transfection to transmembrane receptor for hepatocyte growth factor. Oncogene 7 (1) : 3–7.