@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 Protein: . @prefix mgi: . @prefix geneProductOf: . @prefix mesh: . @prefix species: . @prefix occursIn: . @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 geneProductOf: mgi:96575; a Protein: . sub:_2 occursIn: mesh:D008099, mesh:D017667, mesh:D018482, species:10090; rdf:object mesh:D007333; rdf:predicate belv:increases; rdf:subject sub:_1; a rdf:Statement . sub:assertion rdfs:label "p(MGI:Insr) -> bp(MESHPP:\"Insulin Resistance\")" . } 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 "Skeletal Muscle. Insulin receptor function has been inhibited in two ways: muscle-specific knockout of the insulin receptor (MIRKO; Bruning et al., 1998) and muscle-specific expression of a dominant-negative mutant insulin receptor (IR-A1134T) in transgenic mice (Moller et al., 1996). In both models, skeletal muscle was insulin resistant when studied in vitro."; prov:wasQuotedFrom pubmed:10199397 . sub:_4 rdfs:label "Selventa" . sub:assertion prov:hadPrimarySource pubmed:10199397; prov:wasDerivedFrom beldoc:, sub:_3 . } sub:pubinfo { this: dct:created "2014-07-03T14:29:46.744+02:00"^^xsd:dateTime; pav:createdBy orcid:0000-0001-6818-334X, orcid:0000-0002-1267-0234 . }