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. 2000 May 1;149(3):741–754. doi: 10.1083/jcb.149.3.741

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© 2000 The Rockefeller University Press

This article is distributed under the terms of an Attribution–Noncommercial–Share Alike–No Mirror Sites license for the first six months after the publication date (see http://www.rupress.org/terms). After six months it is available under a Creative Commons License (Attribution–Noncommercial–Share Alike 4.0 Unported license, as described at http://creativecommons.org/licenses/by-nc-sa/4.0/).

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Model of the FN-dependent matrix survival pathway activated in primary RSF when serum is absent. FN supports the organization of a pro-survival signaling complex based on a FAK/Cas scaffold located at focal adhesion sites. Paxillin (Pax) is thought to participate in the binding of FAK to focal adhesion sites (Tachibana et al. 1995). Cas is recruited to the survival complex via a FAK PR-1–Cas SH3 interaction. Matrix survival signaling also requires an intact Cas SD. FN-FAK–associated survival signals activate Ras, and are propagated further via a Rac1/Pak1/MKK4/JNK signaling module, with pJNK detected in focal contacts as well as in the nucleus. This pathway is distinct from the serum-dependent survival pathway that is activated when matrix is withdrawn. The latter pathway requires FAK, but it also requires PI3-kinase, whereas the FN-FAK pathway described herein does not.