||The C-terminal Src kinase (Csk) phosphorylates and downregulates Src family tyrosine kinases Cell transformation by src oncoproteins is caused by several oncogenic mechanisms, which interfere with this phosphorylation. The CSK gene could therefore potentially function as an antioncogene. The Csk-binding protein (Cbp) localizes Csk close to its substrates at the plasma membrane, and increasesthe specific activity of the kinase. It has been reported prior to occurrence of neoplastic lesions in the colon carcinogenesis; the tumor suppressor gene CterminalSrc kinase (Csk) was down-regulated with a concomitant increase in Src activity. Furthermore, pharmacological or genetic (RNA interference) inhibition of Csk resultedin increased proliferation in colon cancer cell lines through the mitogen-activated protein kinase dependent pathway. Csk, which phosphorylates tyrosine residues in the negative regulatory sites of Src family kinases, downregulated Fyn- and Lck-mediated stimulation of the serum response element and Fynmediated enhancement of IL-2 promoter activity.
||100 ng of CSK are sufficient to phosphorylated 1 ug of heat-inactivated nuclear or cytoplasmic extract at 30℃ for 30 mins.
||For in vitro use only.
||Liquid. Supplied in 20 mM Tris-HCl pH 8.0, 100 mM KCl, 0.2 mM EDTA, 1 mM DTT and 20% glycerol.
||20-200 ng are sufficient for an in vitro transcription assay and 100 ng are sufficient for a protein-protein interaction assay.
||> 95% by SDS-PAGE.
||Quality guaranteed for 12 months, Store at -80℃. Avoid freeze / thaw cycles.