@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 go: . @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 occursIn: mesh:D008099, mesh:D017667, mesh:D018482, species:10090; rdf:object go:0030073; rdf:predicate belv:increases; rdf:subject schem:serum%20insulin; a rdf:Statement . sub:assertion rdfs:label "a(SCHEM:\"serum insulin\") -> bp(GO:\"insulin secretion\")" . } 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:_3; pav:version "1.4" . sub:_2 prov:value "Two mechanisms have been identified to explain how insulin receptors promote insulin secretion in b cells. Insulin stimulates exocytosis of secretory vesicles (Aspinwall et al., 1999); exocytosis of insulin feeds back to promote transcription of the insulin gene, an effect mediated by insulin receptors, IRS2, and PI 3-kinase (Leibiger et al., 1998). This role for IRS2 in b cells helps to explain the observation that IRS2 knockout mice developed diabetes because of failure of insulin secretion to compensate for insulin resistance"; prov:wasQuotedFrom pubmed:10199397 . sub:_3 rdfs:label "Selventa" . sub:assertion prov:hadPrimarySource pubmed:10199397; prov:wasDerivedFrom beldoc:, sub:_2 . } sub:pubinfo { this: dct:created "2014-07-03T14:29:46.754+02:00"^^xsd:dateTime; pav:createdBy orcid:0000-0001-6818-334X, orcid:0000-0002-1267-0234 . }