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All rights reserved. http://resource.belframework.org/belframework/20131211/knowledge/large_corpus.bel http://purl.org/dc/elements/1.1/title BEL Framework Large Corpus Document http://resource.belframework.org/belframework/20131211/knowledge/large_corpus.bel http://purl.org/pav/authoredBy http://www.tkuhn.ch/bel2nanopub/RAZIrSYs7cl7zFLzjkOajXb5jkmTTk7bd07kBrS1D6Qgc#_4 http://resource.belframework.org/belframework/20131211/knowledge/large_corpus.bel http://purl.org/pav/version 20131211 http://www.tkuhn.ch/bel2nanopub/RAZIrSYs7cl7zFLzjkOajXb5jkmTTk7bd07kBrS1D6Qgc#_3 http://www.w3.org/ns/prov#value Very recent studies have suggested possible connections between Akt, PTEN, and integrin biology. For example, integrin- airlinked kinase (ILK) activation is inhibited by blockade of Akt function (Persad et al., 2000), and PTEN interacts with focal adhesion kinase (FAK) and influences cell migration (Tamura et al., 1999). These interactions affect cell survival, an event influenced by both VEGF and integrins. Also, cell migration and angiogenesis are reg- ulated by Akt and PTEN, and these cellular responses are clearly mediated by integrins (Jiang et al., 2000). By overexpression approaches, we have directly impli- cated Akt and PTEN in the pathway from VEGF to integ- rin activation. 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