HGFR/c-MET Antibody [Alexa Fluor® 532]

• Reactivity: Hu
• Applications: WB, IHC, ICC/IF
• Clonality: Polyclonal
• Host: Rabbit
• Conjugate: Alexa Fluor 532

HGFR/c-MET Antibody [Alexa Fluor® 532] Summary

• Immunogen: Phosphopeptide containing human HGF R Y1003 site
• Specificity: Detects human and mouse HGF R/c-MET when phosphorylated at Y1003.
• Isotype: IgG
• Clonality: Polyclonal
• Host: Rabbit
• Purity Statement: Antigen Affinity-purified

Applications/Dilutions

• Dilutions:
  • Immunocytochemistry
  • Immunohistochemistry
  • Western Blot

Packaging, Storage & Formulations

• Storage: Protect from light. Do not freeze. 12 months from date of receipt, 2 to 8 °C as supplied
• Buffer: Supplied 0.2mg/ml in 1X PBS with RDF1 and 0.09% Sodium Azide

Notes

This product is produced by and ships from R&D Systems, Inc., a Bio-Techne brand.

Alternate Names for HGFR/c-MET Antibody [Alexa Fluor® 532]

• AUTS9
• cMET
• c-MET
• EC 2.7.10
• EC 2.7.10.1
• hepatocyte growth factor receptor
• HGF R
• HGF receptor
• HGF/SF receptor
• HGFR
• Met (c-Met)
• met proto-oncogene (hepatocyte growth factor receptor)
• met proto-oncogene tyrosine kinase
• MET
• oncogene MET
• Proto-oncogene c-Met
• RCCP2
• Scatter factor receptor
• SF receptor
• Tyrosine-protein kinase Met

Background

HGF R, also known as Met (from N-methyl-N’-nitro-N-nitrosoguanidine induced), is a glycosylated receptor tyrosine kinase that plays a central role in epithelial morphogenesis and cancer development. HGF R is synthesized as a single chain precursor which undergoes cotranslational proteolytic cleavage. This generates a mature HGF R that is a disulfide-linked dimer composed of a 50 kDa extracellular alpha chain and a 145 kDa transmembrane beta chain (1, 2). The extracellular domain (ECD) contains a seven bladed beta -propeller sema domain, a cysteine-rich PSI/MRS, and four Ig-like E-set domains, while the cytoplasmic region includes the tyrosine kinase domain (3, 4). Proteolysis and alternate splicing generate additional forms of human HGF R which either lack of the kinase domain, consist of secreted extracellular domains, or are deficient in proteolytic separation of the alpha and beta chains (5 - 7). The sema domain, which is formed by both the alpha and beta chains of HGF R, mediates both ligand binding and receptor dimerization (3, 8). Ligand-induced tyrosine phosphorylation in the cytoplasmic region activates the kinase domain and provides docking sites for multiple SH2-containing molecules (9, 10). HGF stimulation induces HGF R downregulation via internalization and proteasome-dependent degradation (11). In the absence of ligand, HGF R forms noncovalent complexes with a variety of membrane proteins including CD44v6, CD151, EGF R, Fas, Integrin alpha 6/ beta 4, Plexins B1, 2, 3, and MSP R/Ron (12 - 19). Ligation of one complex component triggers activation of the other, followed by cooperative signaling effects (12 - 19). Formation of some of these heteromeric complexes is a requirement for epithelial cell morphogenesis and tumor cell invasion (12, 16, 17). Paracrine induction of epithelial cell scattering and branching tubulogenesis results from the stimulation of HGF R on undifferentiated epithelium by HGF released from neighboring mesenchymal cells (20). Genetic polymorphisms, chromosomal translocation, overexpression, and additional splicing and proteolytic cleavage of HGF R have been described in a wide range of cancers (1). Within the ECD, human HGF R shares 86% - 88% aa sequence identity with canine, mouse, and rat HGF R.

Limitations

This product is for research use only and is not approved for use in humans or in clinical diagnosis. Primary Antibodies are guaranteed for 1 year from date of receipt.