CSK Protein, Mouse, Recombinant

CSK Protein, Mouse, Recombinant is expressed in Baculovirus insect cells. The predicted molecular weight is 50.9 kDa and the accession number is P41241.

CSK Protein, Mouse, Recombinant

パッケージサイズ	在庫状況	単価(税別)
50 μg	約5 days	￥ 114,500

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説明	CSK Protein, Mouse, Recombinant is expressed in Baculovirus insect cells. The predicted molecular weight is 50.9 kDa and the accession number is P41241.

Species	Mouse
Expression Host	Baculovirus Insect Cells
Tag	Tag Free
Accession Number	P41241
別名	c-src tyrosine kinase, AW212630, p50CSK
Construction	The Mouse CSK (P41241 ) (Met 1-Leu 450) was expressed and purified with two additional amino acids (Gly & Pro ) at the N-terminus.
Protein Purity	> 90 % as determined by SDS-PAGE
分子量	50.9 kDa (predicted)

Endotoxin	< 1.0 EU/μg of the protein as determined by the LAL method.
Formulation	Supplied as sterile 20 mM Tris, 500 mM NaCl, 10% glycerol, pH 8.0.
Reconstitution	A Certificate of Analysis (CoA) containing reconstitution instructions is included with the products. Please refer to the CoA for detailed information.
Stability & Storage	It is recommended to store the product under sterile conditions at -20℃ to -80℃. Samples are stable for up to 12 months. Please avoid multiple freeze-thaw cycles and store products in aliquots.
Shipping	Kinases are highly recommended to be shipped at frozen temperature with blue ice or dry ice.
Research Background	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

参考文献

1. Brauninger A. et al.,1992, Gene. 110: 205-11. 2. Sondhi D. et al., 1999, Biochemistry. 38 (34): 11147-55. 3. Ogawa A. et al., 2002, J Biol Chem. 277 (17): 14351-4. 4. Cole PA. et al., 2003, Curr Opin Chem Biol. 7 (5): 580-5. 5. Baumeister U. et al., 2005,EMBO J. 24 (9): 1686-95.

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CSK Protein, Mouse, Recombinant

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