FAK, phosphorylated (Tyr397), Human (Focal Adhesion Associated Protein Tyrosine Kinase, BC3) BioAssay(TM) ELISA Kit

Focal Adhesion Kinase (FAK), also known as pp125FAK and FADK 1 (EC,2.7.1.112) is a non-receptor protein-tyrosine kinase that localizes to focal adhesions. FAK appears to be ubiquitously expressed among all mammalian tissues, with highest expression levels observed in brain tissue. FAK plays a central role in cell spreading, differentiation, migration, cell death and acceleration of the G1 to S phase transition of the cell cycle. FAK

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SPECIFICATIONS

Catalog Number

F0019-55H

Size

96Tests

Applications

ELISA

References

1. Crowe, D.L., et al. (2004) Recruitment of focal adhesion kinase and paxillin to beta1 integrin promotes cancer cell migration via mitogen activated protein kinase activation. BMC Cancer 4:18.\n2. Cary, L.A., et al. (1996) Stimulation of cell migration by overexpression of focal adhesion kinase and its association with Src and Fyn. J. Cell. Sci. 109:1787-1794.\n3. Igishi, T., et al. (1999) Divergent signaling pathways link focal adhesion kinase to mitogen-activated protein kinase cascades. Evidence for a role of paxillin in c-Jun NH(2)-terminal kinase activation. J. Biol. Chem. 1999 274:30738-30746.\n4. Jones, G., et al. (2001) Loss of focal adhesion kinase (FAK) inhibits epidermal growth factor receptor-dependent migration and induces aggregation of nh(2)-terminal FAK in the nuclei of\napoptotic glioblastoma cells. Cancer Res. 61:4978-4981.\n5. Lee, J.W., et al. (2003) The C-terminal domain of focal adhesion kinase reduces the tumor cell invasiveness in chondrosarcoma cell lines. J. Orthop. Res. 21:1071-1080.\n6. Owen, J.D., et al. (1999) Induced focal adhesion kinase (FAK) expression in FAK-null cells enhances cell spreading and migration requiring both auto- and activation loop phosphorylation sites and inhibits adhesion-dependent tyrosine phosphorylation of Pyk2. Mol. Cell. Biol. 19:4806-4818.\n7. Ruest, P.J., et al. (2000) Phosphospecific antibodies reveal focal adhesion kinase activation loop phosphorylation in nascent and mature focal adhesions and requirement for the autophosphorylation site. Cell Growth Differ. 11:41-48.\n8. Sieg, D.J., et al. (1999) Required role of focal adhesion kinase (FAK) for integrin-stimulated cell migration. J. Cell Sci. 112:2677-2691.\n9. Streblow, D.N., et al. (2003) Human cytomegalovirus chemokine receptor US28-induced smooth muscle cell migration is mediated by focal adhesion kinase and Src. J. Biol. Chem. 278:50456-50465.\n10. Xu, L.H., et al. (2004) The focal adhesion kinase suppresses transformation-associated, anchorage-independent apoptosis in human breast cancer cells. J. Biol. Chem. 275:30597-30604.\n11. Yu, H.G., et al. (2004) Rapid tyrosine phosphorylation of focal adhesion kinase, paxillin, and p130Cas by gastrin in human colon cancer cells. Biochem. Pharmacol. 67:135-146.

Additional Info

FAK [pY397] ELISA recognizes human, rat, and mouse FAK. Other species have not been tested. The specificity of this assay for phosphorylated FAK [pY397] was confirmed by peptide competition. The data show that only the phospho-peptide containing the phosphorylated tyrosine 397 could block the ELISA signal. The non-phosphorylated peptide sequence or other phosphopeptides from the FAK sequence did not block the signal.