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First published online January 21, 2009

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FAK divides and conquers

An inappropriate ECM environment can induce a form of apoptosis termed anoikis. Several studies using a variety of cell types have shown that focal adhesion kinase (FAK), a key mediator of integrin signalling, has a crucial role in suppressing anoikis – but many different integrins can activate FAK, so how are the cell-type-specific effects regulated? On page 357, Andrew Gilmore, Charles Streuli and colleagues use a constitutively active form of FAK to examine the mechanism by which FAK signals to suppress anoikis in mouse fibroblasts and epithelial cells, which have distinct embryonic lineages. The authors show that ECM-derived survival signals are commonly transduced by FAK in fibroblasts and epithelial cells, but the activation of FAK is interpreted differently in each cell type. The adaptor protein p130cas is shown to be a key downstream component of the FAK signalling pathway, promoting survival in fibroblasts but not in epithelial cells, in agreement with previous studies. By contrast, however, paxillin binding and tyrosine-925 phosphorylation of FAK are crucial events that are associated with FAK-dependent survival in epithelial cells. Thus, the authors conclude, cellular context is an important aspect in determining how the same survival signal is interpreted intracellularly.

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Related articles in JCS:

FAK engages multiple pathways to maintain survival of fibroblasts and epithelia – differential roles for paxillin and p130Cas

Nadia K. Zouq, James A. Keeble, Jennefer Lindsay, Anthony J. Valentijn, Lu Zhang, Deborah Mills, Christopher E. Turner, Charles H. Streuli, and Andrew P. Gilmore
JCS 2009 122: 357-367. [Abstract] [Full Text]  

This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Related articles in JCS Similar articles in this journal Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Search for Related Content Social Bookmarking                         What's this?