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All rights reserved. http://resource.belframework.org/belframework/1.0/knowledge/large_corpus.bel http://purl.org/dc/elements/1.1/title BEL Framework Large Corpus Document http://resource.belframework.org/belframework/1.0/knowledge/large_corpus.bel http://purl.org/pav/authoredBy http://www.tkuhn.ch/bel2nanopub/RAGSXdAIDT1FAzjwbZ2jnhYwwHst8b8smgb94zzGzJLwY#_3 http://resource.belframework.org/belframework/1.0/knowledge/large_corpus.bel http://purl.org/pav/version 1.4 http://www.tkuhn.ch/bel2nanopub/RAGSXdAIDT1FAzjwbZ2jnhYwwHst8b8smgb94zzGzJLwY#_2 http://www.w3.org/ns/prov#value Although several lines of evidence show an important link between cytoskeletal integrity and cell viability, the molecular mechanisms for this link are likely to be numerous. In a broad sense, they may separate into two classes of events, either primarily mechanical or chemical. In the latter, signaling molecules or enzymes essential for nuclear or cytoplasmic breakdown are sequestered or inhibited by the cytoskeleton. Disruption of the cytoskeleton by any means would then liberate or activate these sequestered elements and allow them to reach their targets. A more directly mechanical role is suggested by the requirement for appropriately arranged extracellular contacts to prevent cell death (35). In this model, the mechanical tension produced at sites of cell-cell or cell-matrix contact is transmitted by an intact cytoskeleton throughout the cell. 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