Name :
Recombinant Human c-MET/HGFR Protein (aa 956-1390, His & GST Tag)

Biological Activity :

Background :
Hepatocyte growth factor receptor (HGFR), also known as c-Met or mesenchymal-epithelial transition factor (MET), is a receptor tyrosine kinase (RTK) that is overexpressed and/or mutated in a variety of malignancies. HGFR protein is produced as a single-chain precursor, and HGF is the only known ligand. Normal HGF/HGFR signaling is essential for embryonic development, tissue repair, or wound healing, whereas aberrantly active HGFR has been strongly implicated in tumorigenesis, particularly in the development of invasive and metastatic phenotypes. HGFR protein is a multifaceted regulator of growth, motility, and invasion, and is normally expressed by cells of epithelial origin. Preclinical studies suggest that targeting aberrant HGFR signaling could be an attractive therapy in cancer. Cancer Immunotherapy Immune Checkpoint Immunotherapy Targeted Therapy

Biological Activity :
1. The specific activity was determined to be 10 nmol/min/mg using MBP as substrate.2. Measured by its binding ability in a functional ELISA. Immobilized human HGFR (aa 956-1390) (Cat: 10692-H20B1) at 10 μg/ml (100 μl/well) can bind biotinylated human HGF-his (Cat: 10463-H08H) with a linear range of 15.6-125 ng/ml.

Expression Host :
Human

Source :
Baculovirus-Insect Cells

Tag :

Protein Accession No. :
P08581-1

NCBI Gene ID :

Synonyms :

Synonyms :
MET proto-oncogene, receptor tyrosine kinase

Amino Acid Sequence :

Molecular Weight :
The recombinant human MET /GST chimera consists of 672 amino acids and has a calculated molecular mass of 76.8 kDa. The recombinant protein migrates as an approximately 68 kDa band in SDS-PAGE under reducing conditions.

Purity :
> 90 % as determined by SDS-PAGE

State of Matter :

Product Concentration :

Storage and Stability :
Samples are stable for up to twelve months from date of receipt at -20℃ to -80℃. Store it under sterile conditions at -20℃ to -80℃. It is recommended that the protein be aliquoted for optimal storage. Avoid repeated freeze-thaw cycles.

Endotoxin Level :
< 1.0 EU per μg of the protein as determined by the LAL method

Protein Construction :
A DNA sequence encoding the human MET (P08581-1) (Lys956-Ser1390) was fused with the N-terminal polyhistidine-tagged GST tag at the N-terminus.

Buffer Solution :
Supplied as sterile 20mM Tris, 500mM NaCl, pH 7.4, 10% glycerol, 3mM DTTPlease contact us for any concerns or special requirements.Please refer to the specific buffer information in the hardcopy of datasheet.

Shipping :
Kinases are highly recommended to be shipped at frozen temperature with blue ice or dry ice.Shipment made at ambient temperature may seriously affect the activity of the ordered products.

Redissolution :
A hardcopy of COA with reconstitution instruction is sent along with the products. Please refer to it for detailed information.

Synonyms :
AUTS9 Protein, Human; c-Met Protein, Human; DFNB97 Protein, Human; HGFR Protein, Human; RCCP2 Protein, Human c-MET/HGFR 背景信息 Hepatocyte growth factor receptor (HGFR), also known as c-Met or mesenchymal-epithelial transition factor (MET), is a receptor tyrosine kinase (RTK) that is overexpressed and/or mutated in a variety of malignancies. HGFR protein is produced as a single-chain precursor, and HGF is the only known ligand. Normal HGF/HGFR signaling is essential for embryonic development, tissue repair, or wound healing, whereas aberrantly active HGFR has been strongly implicated in tumorigenesis, particularly in the development of invasive and metastatic phenotypes. HGFR protein is a multifaceted regulator of growth, motility, and invasion, and is normally expressed by cells of epithelial origin. Preclinical studies suggest that targeting aberrant HGFR signaling could be an attractive therapy in cancer. Cancer Immunotherapy Immune Checkpoint Immunotherapy Targeted Therapy

References & Citations :
McGill GG, et al. (2006) c-Met expression is regulated by Mitf in the melanocyte lineage. J Biol Chem. 281(15): 10365-73. Garcia S, et al. (2007) c-Met overexpression in inflammatory breast carcinomas: automated quantification on tissue microarrays. British journal of cancer. 96(2): 329-35. Socoteanu MP, et al. (2008) c-Met targeted therapy of cholangiocarcinoma. World J Gastroenterol. 14(19): 2990-4. Kong DS, et al. (2009) Prognostic significance of c-Met expression in glioblastomas. Cancer. 115(1): 140-8.

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