c-Met (del 963-1009) Kinase Assay Kit
The c-Met (del 963-1009) Kinase Assay Kit is designed to measure the kinase activity of c-Met (del 963-1009, exon 14 deletion) for screening and profiling applications using Kinase-Glo® MAX as a detection reagent. The recombinant protein used in the kit corresponds to amino acids 956-1390 of c-Met that contain the tyrosine kinase domain. The recombinant protein also contains a deletion of amino acids 963-1009 corresponding to exon 14 skipping.
Kinase-Glo MAX (Promega #V6071)
Dithiothreitol (DTT, 1 M; optional)
Microplate reader capable of reading luminescence
Adjustable micropipettor and sterile tips
30°C incubator
| Catalog Number |
Reagent |
Amount |
Storage |
| 100643 | c-Met (del 963-1009), GST-tag* | 2.5 µg | -80°C |
| 79334 | 5x Kinase assay buffer | 1.5 ml | -20°C |
| 79686 | ATP (500 μM) | 100 µl | -20°C |
| 40217 | PTK substrate, Poly (Glu:Tyr, 4:1) (10 mg/ml) | 100 µl | -20°C |
| 79696 | 96-well plate, white | 1 | Room Temp |
*The concentration of the protein is lot-specific and will be indicated on the tube
c-Met, also known as HGFR (hepatocyte growth factor receptor), is a tyrosine kinase receptor encoded by the gene MET. Upon binding its ligand HGF (hepatocyte growth factor), c-Met activates multiple cellular processes including proliferation, adhesion and angiogenesis. Importantly, c-Met is overexpressed in various carcinomas, suggesting that HGF/c-Met signaling pathway could be a promising target for cancer treatment. A splice mutation that results in skipping exon 14 has been identified in the tumor tissue of approximately 4% of patients with lung cancer, particularly those with non-small cell lung cancer. This mutation causes over-expression of MET protein and increased MET activation, leading to oncogenesis.
Recondo G. et al. Targeting MET Dysregulation in Cancer. Cancer Discov. 2020; 10(7): 922-934. Review.
Awad, M.M., et al. "MET exon 14 mutations in non–small-cell lung cancer are associated with advanced age and stage-dependent MET genomic amplification and c-Met overexpression." J. Clin. Oncology 2016; 34: 721-30.
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