HGF R/c-MET Antibody (SP59) Summary
| Immunogen |
Synthetic peptide corresponding to the region of c-Met that contains non-phosphorylated tyrosine1003
|
| Localization |
Membrane
|
| Isotype |
IgG
|
| Clonality |
Monoclonal
|
| Host |
Rabbit
|
| Gene |
MET
|
| Purity |
Protein A purified
|
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|
Applications/Dilutions
| Dilutions |
|
| Application Notes |
For IHC-P antigen retrieval, boil tissue section in 10mM citrate buffer, pH 6.0 for 10 min followed by cooling at room temperature for 20 min.
|
Packaging, Storage & Formulations
| Storage |
Store at 4C. Do not freeze.
|
| Buffer |
7.0 ml prediluted antibody with PBS (pH 7.6) and 1.0% BSA
|
| Preservative |
0.1% Sodium Azide
|
| Purity |
Protein A purified
|
Notes
For a positive control use Breast carcinoma.
Alternate Names for HGF R/c-MET Antibody (SP59)
- 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
Met is a receptor protein-tyrosine kinase (RPTK) for hepatocyte growth factor (HGF), which is a multifunctional cytokine controlling cell growth, morphogenesis, and motility. Met overexpression has been identified in a variety of human cancers (1). Met kinase domain possesses unique features that distinguish met from other members of the src family of protein tyrosine kinases. These results also demonstrate that the product of the activated met gene is a fusion protein and that the amino terminal end of this fusion protein exhibits homology to laminin B1 (2). Data suggest that RanBP9, functioning as an adaptor protein for the Met tyrosine kinase domain, can augment the HGF-Met signaling pathway and that RanBP9 overexpression may cause constitutive activation of the Ras signaling pathway (1). Hereditary papillary renal carcinoma (HPRC) is a recently recognized form of inherited kidney cancer Results suggest that missense mutations located in the MET proto-oncogene lead to constitutive activation of the Met protein and papillary renal carcinomas (3)