Anti-C-Src Kinase / CSK antibody

Anti-C-Src Kinase / CSK antibody

• DataSheet
• Material Safety Data Sheets (MSDS)

Rabbit polyclonal to C-Src Kinase / CSK

ELISA, WB

Mouse C-Src Kinase / CSK

AW212630 antibody; Csk antibody; CSK antibody; c-Src Kinase antibody; c-Src Kinase antibody; c-Src tyrosine kinase antibody; c-Src tyrosine kinase antibody; MGC117393 antibody; p50CSK antibody; AW212630 antibody; Src antibody; SRC antibody

Rabbit IgG

Produced in rabbits immunized with purified, recombinant Mouse C-Src Kinase / CSK (rh C-Src Kinase / CSK; P41241; Met1-Leu450). C-Src Kinase / CSK specific IgG was purified by Mouse C-Src Kinase / CSK affinity chromatography.

Polyclonal

0.2 μm filtered solution in PBS

This antibody can be stored at 2℃-8℃ for one month without detectable loss of activity. Antibody products are stable for twelve months from date of receipt when stored at -20℃ to -80℃. Preservative-Free.
Sodium azide is recommended to avoid contamination (final concentration 0.05%-0.1%). It is toxic to cells and should be disposed of properly. Avoid repeated freeze-thaw cycles.

The tyrosine kinase c-Src has been implicated as a modulator of cell proliferation, spreading, and migration. These functions are also regulated by Met. The structure of a large fragment of the c-Src kinase comprises the regulatory and kinase domains and the carboxy-terminal tall. c-Src kinase interactions among domains and is stabilized by binding of the phosphorylated tail to the SH2 domain. This molecule is locked in a conformation that simultaneously disrupts the kinase active site and sequesters the binding surfaces of the SH2 and SH3 domains. The structure shows how appropriate cellular signals, or transforming mutations in v-Src, could break these interactions to produce an open, active kinase. The protein-tyrosine kinase activity of c-Src kinase is inhibited by phosphorylation of tyr527, within the c-Src c-terminal tail. Genetic and biochemical data have suggested that this negative regulation requires an intact Src homology 2 (SH2) domain. Since SH2 domains recognize phosphotyrosine, it is possible that these two non-catalytic domains associate, and thereby repress c-Src kinase activity. Experiments have suggested that c-Src kinase plays a role in the biological behaviour of colonic carcinoma cells induced by migratory factors such as EGF, perhaps acting in conjunction with FAK to regulate focal adhesion turnover and tumour cell motility. Furthermore, although c-Src kinase has been implicated in colonic tumour progression, in the adenoma to carcinoma in vitro model c-Src is not the driving force for this progression but co-operates with other molecules in carcinoma development. References

• Brauninger A. et al.,1992, Gene. 110: 205-11.
• Sondhi D. et al., 1999, Biochemistry. 38 (34): 11147-55.
• Ogawa A. et al., 2002, J Biol Chem. 277 (17): 14351-4.
• Cole PA. et al., 2003, Curr Opin Chem Biol. 7 (5): 580-5.
• Baumeister U. et al., 2005,EMBO J. 24 (9): 1686-95.