|Application ||WB, IF|
|Reactivity||Human, Mouse, Rat|
|Calculated MW||33831 Da|
|Other Names||Adapter molecule crk, Proto-oncogene c-Crk, p38, CRK|
|Target/Specificity||A synthetic peptide corresponding to residues in the second SH3 domain and near C-terminus of human Crk (p38) protein was used as immunogen.|
|Format||50 mM Tris-Glycine (pH 7.4), 0.15 M NaCl, 40% Glycerol, 0.01% sodium azide and 0.05% BSA.|
|Storage||Maintain refrigerated at 2-8°C for up to 6 months. For long term storage store at -20°C in small aliquots to prevent freeze-thaw cycles.|
|Precautions||Crk/p38 Antibody is for research use only and not for use in diagnostic or therapeutic procedures.|
|Function||The Crk-I and Crk-II forms differ in their biological activities. Crk-II has less transforming activity than Crk-I. Crk- II mediates attachment-induced MAPK8 activation, membrane ruffling and cell motility in a Rac-dependent manner. Involved in phagocytosis of apoptotic cells and cell motility via its interaction with DOCK1 and DOCK4. May regulate the EFNA5-EPHA3 signaling.|
|Cellular Location||Cytoplasm. Cell membrane. Note=Translocated to the plasma membrane upon cell adhesion.|
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Provided below are standard protocols that you may find useful for product applications.
Crk (p38) are adaptor proteins, composed mostly of SH2 and SH3 domains, which play a key role in cellular signaling by mediating the construction of protein complexes and also by managing cell proliferation, differentiation, and migration (1). They are critical integrators of upstream signals for cell invasion and migration in human cancer cell lines. Crk is believed to be a regulator of invasive responses because increased levels of the protein have been observed in multiple human cancers (2). In vivo studies have demonstrated that decreased levels of Crk remarkably inhibits tumor formation and its invasive growth (3). Crk associates with ERM family proteins (including ezrin, radixin, and moesin), activates RhoA, and promotes cell motility toward hyaluronic acid (4).
1. Nishihara H, et al. Cancer Lett (1):55-61, 2002
2. Watanabe T, et al. Mol Cancer Res. (7):499-510, 2006
3. Rodrigues SP, et al. Mol Cancer Res. (4):183-94, 2005
4. Tsuda MJ, et al. Biol Chem. (45):46843-50, 2004
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