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Sci. Signal., 20 May 2008
Vol. 1, Issue 20, p. pe22
[DOI: 10.1126/stke.120pe22]


Focal Adhesion Kinase Versus p53: Apoptosis or Survival?

William G. Cance1,2,3* and Vita M. Golubovskaya1,2*

1Department of Surgery, University of Florida, School of Medicine, Gainesville, FL 32610, USA.
2University of Florida Shands Cancer Center, University of Florida, Gainesville, FL 32610, USA.
3Department of Biochemistry and Molecular Biology, University of Florida, Gainesville, FL 32610, USA.

Abstract: Focal adhesion kinase (FAK) is a tyrosine kinase that interacts with a multitude of signaling partners and helps cells to survive in the face of various proapoptotic signals. One of the most important interactions for FAK is with the tumor suppressor protein p53. p53 binds not only to the amino-terminal domain of FAK but also to the FAK promoter to inhibit its transcription. A study now reports the biological implications of the kinase-independent interaction of FAK with p53, which opens up future perspectives in cell signaling and cancer research. We focus on FAK and p53 signaling, which link signal transduction pathways from the extracellular matrix and cytoplasm to the nucleus, in human and mouse cells. FAK is proposed to be a critical scaffold protein that sequesters proapoptotic proteins, such as p53, to mediate cell survival.

*Corresponding authors. Department of Surgery, Health Science Center, Post Office Box 100286, 1600 Southwest Archer Road, Gainesville, FL 32610–0286, USA. E-mail, cance{at} (W.G.C.); golubvi{at} (V.M.G.).

Citation: W. G. Cance, V. M. Golubovskaya, Focal Adhesion Kinase Versus p53: Apoptosis or Survival? Sci. Signal. 1, pe22 (2008).

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