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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/RAx1trIZw04_u6XW3v9QYRX7J-4wqDjawA5PiIAWo_XGg#_6 http://resource.belframework.org/belframework/1.0/knowledge/large_corpus.bel http://purl.org/pav/version 1.4 http://www.tkuhn.ch/bel2nanopub/RAx1trIZw04_u6XW3v9QYRX7J-4wqDjawA5PiIAWo_XGg#_5 http://www.w3.org/ns/prov#value In unstimulated cells, GSK3 is active and contributes significantly towards the phosphorylation and inhibition of glycogen synthase [12]. Insulin stimulates glycogen synthesis both by inactivating GSK3 and also by promoting the dephosphorylation of glycogen synthase. The inactivation of GSK3 and GSK3 is achieved through phosphorylation of Ser21 and Ser9, respectively [12], and this is mediated by PKB in a PI3K-dependent fashion. Thus PI3K, PDK, PKB and GSK3 constitute one important arm of the insulin signalling cascade regulating glycogen synthesis. 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