@prefix this: . @prefix sub: . @prefix beldoc: . @prefix rdfs: . @prefix rdf: . @prefix xsd: . @prefix dct: . @prefix dce: . @prefix pav: . @prefix np: . @prefix belv: . @prefix prov: . @prefix schem: . @prefix pfh: . @prefix proteinModification: . @prefix psimod: . @prefix species: . @prefix occursIn: . @prefix mesh: . @prefix pubmed: . @prefix orcid: . sub:Head { this: np:hasAssertion sub:assertion; np:hasProvenance sub:provenance; np:hasPublicationInfo sub:pubinfo; a np:Nanopublication . } sub:assertion { sub:_1 belv:variantOf pfh:AKT%20Family; a proteinModification:, psimod:00696 . sub:_2 occursIn: mesh:D009130, mesh:D017667, species:9606; rdf:object sub:_1; rdf:predicate belv:increases; rdf:subject schem:serum%20insulin; a rdf:Statement . sub:assertion rdfs:label "a(SCHEM:\"serum insulin\") -> p(PFH:\"AKT Family\",pmod(P))" . } sub:provenance { beldoc: dce:description "Approximately 61,000 statements."; dce:rights "Copyright (c) 2011-2012, Selventa. All rights reserved."; dce:title "BEL Framework Large Corpus Document"; pav:authoredBy sub:_4; pav:version "1.4" . sub:_3 prov:value "Inhibition of PI3-kinase activity using a dominant negative mutant (30), or pharmacological agents such as wortmannin or LY294002 (31), abolishes insulin stimulated glucose uptake and inhibits GLUT4 vesicle translocation to the plasma membrane. Many other cellular effects of insulin, such as antilipolysis, activation of fatty acid synthesis, acetyl CoA-carboxylase, glycogen synthase, Akt phosphorylation, glycogen synthase kinase 3b inactivation, and stimulation of protein synthesis and DNA synthesis, are also inhibited by PI3- kinase suppression PIP3, rather than PIP2, is the major mediator of PI3- kinase dependent biological actions of insulin"; prov:wasQuotedFrom pubmed:10194465 . sub:_4 rdfs:label "Selventa" . sub:assertion prov:hadPrimarySource pubmed:10194465; prov:wasDerivedFrom beldoc:, sub:_3 . } sub:pubinfo { this: dct:created "2014-07-03T14:29:46.502+02:00"^^xsd:dateTime; pav:createdBy orcid:0000-0001-6818-334X, orcid:0000-0002-1267-0234 . }