CycLex Met Kinase Assay/Inhibitor Screening Kit

Other - 1) Screening inhibitors or activators of recombinant catalytic domain of Met. 2) Detecting the effects of pharmacological agents on recombinant catalytic domain of Met.

The CycLex® Met Kinase Assay/Inhibitor Screening kit is designed to measure the activities of recombinant catalytic domain of Met for the rapid and sensitive evaluation of inhibitors or activators. The phosphotyrosine specific monoclonal antibody used in this assay kit specifically recognizes the phosphotyrosine residue in the recombinant catalytic domain of Met, which is captured and activated by recombinant ?Tyrosine kinase-binding module-1? (Cat. No. CY-2080) that has been immobilized on a microtiter plate.

Rat: 17295

The MET protooncogene was discovered because of the ability of oncogenic Met to mediate chemically induced transformation of a human osteogenic sarcoma cell line (1). This receptor tyrosine kinase is synthesized as a single-chain precursor, which undergoes intracellular proteolytic cleavage at a basic amino acid site, yielding a disulfide-linked heterodimer. Its C-terminal, intracellular region contains a multifunctional docking site that binds to various signaling molecules. The ligand of the Met receptor is HGF/scatter factor, known to stimulate invasive growth of epithelial cells (2). It is a multifunctional factor affecting a number of cell targets including epithelium, endothelium, myoblasts, spinal motor neurons, and hematopoietic cells. Signaling pathways activated by the HGF-Met interaction mediate cell adhesion and motility. These cellular phenotypes, coupled to tightly regulated changes in cell growth, morphology, and survival, define a general pattern of invasive growth that occurs widely in normal development. In addition, Met is involved in malignant cell transformation. Increased Met expression has been found in a significant percentage of human cancers and is amplified during the transition between primary tumors and metastasis. Point mutations in MET have been identified in hereditary and sporadic papillary renal carcinomas (3?5), hepatocellular and gastric carcinomas (6, 7), and head and neck squamous carcinomas (8). Numerous experimental and clinical data indicate a particular role of HGF and Met in tumor invasive growth, a stage of tumor progression leading to metastases. Dysregulation of Met activity in cells is thought to be a key event underlying tumor metastasis, and indeed, Met overexpression and hyperactivation are reported to correlate with metastatic ability of the tumor cells (9).

Microplate, 10X Wash Buffer, Kinase Buffer, 20X ATP HRP conjugated Detection Antibody Substrate Reagent, Stop Solution

Met