| Autor: |
Playford MP; Department of Cell and Developmental Biology, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599, USA., Vadali K, Cai X, Burridge K, Schaller MD |
| Jazyk: |
angličtina |
| Zdroj: |
Experimental cell research [Exp Cell Res] 2008 Oct 15; Vol. 314 (17), pp. 3187-97. Date of Electronic Publication: 2008 Aug 23. |
| DOI: |
10.1016/j.yexcr.2008.08.010 |
| Abstrakt: |
Focal Adhesion Kinase (FAK) is a non-receptor tyrosine kinase that plays a key role in cellular processes such as cell adhesion, migration, proliferation and survival. Recent studies have also implicated FAK in the regulation of cell-cell adhesion. Here, evidence is presented showing that siRNA-mediated suppression of FAK levels in NBT-II cells and expression of dominant negative mutants of FAK caused loss of epithelial cell morphology and inhibited the formation of cell-cell adhesions. Rac and Rho have been implicated in the regulation of cell-cell adhesions and can be regulated by FAK signaling. Expression of active Rac or Rho in NBT-II cells disrupted formation of cell-cell contacts, thus promoting a phenotype similar to FAK-depleted cells. The loss of intercellular contacts in FAK-depleted cells is prevented upon expression of a dominant negative Rho mutant, but not a dominant negative Rac mutant. Inhibition of FAK decreased tyrosine phosphorylation of p190RhoGAP and elevated the level of GTP-bound Rho. This suggests that FAK regulates cell-cell contact formation by regulation of Rho. |
| Databáze: |
MEDLINE |
| Externí odkaz: |
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