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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/RAyiValnzfwmct2LY7Jf1wr6q0BdXJll76TJfhrSUxToQ#_6 http://resource.belframework.org/belframework/20131211/knowledge/large_corpus.bel http://purl.org/pav/version 20131211 http://www.tkuhn.ch/bel2nanopub/RAyiValnzfwmct2LY7Jf1wr6q0BdXJll76TJfhrSUxToQ#_5 http://www.w3.org/ns/prov#value Akt plays a central role in controlling cell growth, proliferation, survival, and differentiation by phosphorylating a diverse number of protein substrates that contain a minimal consensus sequence of RXRXXS/T (Scheid and Woodgett, 2001). Among these are proteins implicated in metabolism, cell growth, and proliferation such as GSK3, mTOR, and TSC2, and proteins that play roles in apoptosis such as BAD, ASK1, and the Forkhead family of transcription factors FoxOs (Lawlor and Alessi, 2001). It is therefore important to understand how Akt can control such a diverse array of cellular functions. Akt is believed to couple the growth-factor-PI3K signaling pathway to the nutrient-regulated TORC1 signaling pathway (Wullschleger et al., 2006). 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