Anti-C-MET/HGFR Antibody
- SPECIFICATION
- CITATIONS
- PROTOCOLS
- BACKGROUND
Application
| WB |
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Primary Accession | P08581 |
Host | Rabbit |
Reactivity | Human, Rat |
Clonality | Polyclonal |
Format | Lyophilized |
Description | Rabbit IgG polyclonal antibody for Hepatocyte growth factor receptor(MET) detection. Tested with WB in Human;Rat. |
Reconstitution | Add 0.2ml of distilled water will yield a concentration of 500ug/ml. |
Gene ID | 4233 |
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Other Names | 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 |
Calculated MW | 155541 MW KDa |
Application Details | Western blot, 0.1-0.5 µg/ml, Rat, Human |
Subcellular Localization | Membrane; Single-pass type I membrane protein. |
Tissue Specificity | 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. . |
Protein Name | Hepatocyte growth factor receptor |
Contents | Each vial contains 5mg BSA, 0.9mg NaCl, 0.2mg Na2HPO4, 0.05mg NaN3. |
Immunogen | 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. |
Purification | Immunogen affinity purified. |
Cross Reactivity | No cross reactivity with other proteins |
Storage | At -20˚C for one year. After r˚Constitution, at 4˚C for one month. It˚Can also be aliquotted and stored frozen at -20˚C for a longer time.Avoid repeated freezing and thawing. |
Sequence Similarities | Belongs to the protein kinase superfamily. Tyr protein kinase family. |
Name | MET |
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Function | 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 neuronal precursors, angiogenesis and kidney formation. During skeletal muscle development, it is crucial for the migration of muscle progenitor cells and for the proliferation of secondary myoblasts (By similarity). In adults, participates in wound healing as well as organ regeneration and tissue remodeling. Promotes also differentiation and proliferation of hematopoietic cells. May regulate cortical bone osteogenesis (By similarity). |
Cellular Location | Membrane; Single-pass type I membrane protein. |
Tissue Location | 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. Expressed in metaphyseal bone (at protein level) (PubMed:26637977). |
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Background
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.
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