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Example sentences for: fak
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In addition, the SH3 domain of Cas mediates an interaction with FAK, C3G, CMS, and the zinc finger containing protein CIZ, while nephrocystin interacts with Cas via its SH3 domain and proline rich sequences in Cas [ 24 25 26 27 28 29 30 ] . The SH3 domain of Cas can also interact with the tyrosine phosphatase PTP1B, and expression of PTP1B in transformed cells reverts the phenotype, in part by dephosphorylating Cas [ 31 32 ] .
Beatrice Knudsen, Weill Medical College of Cornell University, NY, NY); anti-FAK and anti-Cas (Transduction Laboratories, Lexington, KY).
One of the established in vivo substrates of PTEN, FAK, is known to play a major role in growth-regulatory signal transduction initiated by cell surface integrin receptors [ 48 49 ] . As we observe a correlation between increased PTEN activity and decreased levels of FAK phosphorylation (compare Figure 4Band Figure 5), it is likely that the dephosphorylation of FAK in response to the disruption of cell-matrix interactions is accomplished by increased PTEN activity.
The cell surface expressed integrins can control this process by physically interacting with the extracellular matrix proteins and other cell surface proteins on endothelial cells lining the blood vessel wall [ 1 ] . These integrins signal adhesion and migration by communicating with several tyrosine kinases inside the cell, including the Focal Adhesion Kinase (FAK) and Src family kinases [ 1 2 ] . Src kinases control the activation of FAK, as well as the tyrosine phosphorylation of critical substrates that regulate adhesion and migration [ 3 ] . Indeed, colon cancer cells with high metastatic potential have elevated levels of Src activity or activating mutations in the Src gene [ 4 5 ] . One Src substrate that is involved in regulating an important signaling node in this process is the adaptor protein p130 cas (Cas) [ 6 7 8 9 10 ] . Cas appears to play a central role in the transformation process by several oncogenes including ras, ornithine decarboxylase (ODC), v-Src, v-crk, and Bcr-Abl, as these tumors all have elevated levels of tyrosine phosphorylated Cas [ 6 11 12 13 ] . Cells from mice that lack Cas have much reduced migration and are resistant to transformation by v-Src, while expression of Cas anti-sense RNA in cells transformed with ras, v-Src or ODC result in reversion of the transformed phenotype [ 11 14 15 ] . Furthermore, increased expression of Cas can rescue cell migration and adhesion in cells expressing the tumor suppressor PTEN, and can enhance cell migration and adhesion in normal cells, with a major role being played by the substrate domain [ 16 17 ] .
For a number of GPCRs, including the lysophosphatidic acid (LPAR) [ 7 ] , β-adrenergic 2 (β 2 -AR) [ 8 ] and μ- and δ-OR receptors [ 9 ] , the activation of a non-receptor tyrosine kinase of the Src or focal adhesion kinase (FAK) [ 10 ] families are involved.
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