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|Tested species reactivity||Human|
|Published species reactivity||Human|
|Host / Isotype||Mouse / IgG2a|
|Immunogen||Synthetic peptide derived from cytoplasmic domain of human c-Met protein.|
|Storage buffer||PBS, pH 7.4|
|Contains||0.1% sodium azide|
|Tested Applications||Dilution *|
|ELISA (ELISA)||Assay Dependent|
|Immunohistochemistry (IHC)||Assay Dependent|
|Immunoprecipitation (IP)||Assay Dependent|
|Western Blot (WB)||Assay Dependent|
* Suggested working dilutions are given as a guide only. It is recommended that the user titrate the product for use in their own experiment using appropriate negative and positive controls.
The c-Met oncogene was originally isolated from a chemical carcinogen-treated human osteogenic sarcoma cell line by transfection analysis in NIH/3T3 cells. The Met proto-oncogene product was identified as a trans-membrane receptor-like protein with tyrosine kinase activity that is expressed in many tissues. The c-Met gene product has been identified as the cell surface receptor for hepatocyte growth factor, a plasminogen-like protein thought to be a humoral mediator of liver regeneration.
For Research Use Only. Not for use in diagnostic procedures. Not for resale without express authorization.
Increase of MET gene copy number confers resistance to a monovalent MET antibody and establishes drug dependence.
37-0100 was used in western blot to study mechanisms underlying resistance to MET monoclonal antibodies and chemical tyrosine kinase inhibitors.
|Martin V,Corso S,Comoglio PM,Giordano S||Molecular oncology (8:1561)||2014|
Gene silencing of c-Met leads to brain metastasis inhibitory effects.
37-0100 was used in immunohistochemistry - frozen section and western blot to investigate the role of c-Met in brain metastasis and test its potential as a preventive and/or therapeutic target in this disease.
|Lee SJ,Seol HJ,Lee HW,Kang WY,Kang BG,Jin J,Jo MY,Jin Y,Lee JI,Joo KM,Nam DH||Clinical & experimental metastasis (30:845)||2013|
Tissue microarray-based studies of patients with lymph node negative breast carcinoma show that met expression is associated with worse outcome but is not correlated with epidermal growth factor family receptors.
||Tolgay Ocal I,Dolled-Filhart M,D'Aquila TG,Camp RL,Rimm DL||Cancer (97:1841)||2003|
AUTS9, RCCP2, c-Met, HGFR
HGF receptor, HGF/SF receptor, SF receptor, hepatocyte growth factor receptor, met proto-oncogene tyrosine kinase, proto-oncogene c-Met, scatter factor receptor, tyrosine-protein kinase Met, EC 18.104.22.168, HGF-SF receptor, Hepatocyte growth factor receptor precursor, Met proto- oncogene tyrosine kinase, c-met, kinase EC 22.214.171.124, Met proto- oncogene tyros