@prefix this: <http://www.tkuhn.ch/bel2nanopub/RASGpvs9BPvVGJ6QXNh7-d34Sm6JGPbt1CNf89O3ngo08> .
@prefix sub: <http://www.tkuhn.ch/bel2nanopub/RASGpvs9BPvVGJ6QXNh7-d34Sm6JGPbt1CNf89O3ngo08#> .
@prefix beldoc: <http://resource.belframework.org/belframework/1.0/knowledge/large_corpus.bel> .
@prefix rdfs: <http://www.w3.org/2000/01/rdf-schema#> .
@prefix rdf: <http://www.w3.org/1999/02/22-rdf-syntax-ns#> .
@prefix xsd: <http://www.w3.org/2001/XMLSchema#> .
@prefix dct: <http://purl.org/dc/terms/> .
@prefix dce: <http://purl.org/dc/elements/1.1/> .
@prefix pav: <http://purl.org/pav/> .
@prefix np: <http://www.nanopub.org/nschema#> .
@prefix belv: <http://www.selventa.com/vocabulary/> .
@prefix prov: <http://www.w3.org/ns/prov#> .
@prefix schem: <http://resource.belframework.org/belframework/1.0/namespace/selventa-legacy-chemical-names/> .
@prefix go: <http://amigo.geneontology.org/amigo/term/GO:> .
@prefix Protein: <http://www.ebi.ac.uk/chebi/searchId.do?chebiId=CHEBI_36080> .
@prefix hgnc: <http://www.genenames.org/cgi-bin/gene_symbol_report?hgnc_id=> .
@prefix geneProductOf: <http://purl.obolibrary.org/obo/RO_0002204> .
@prefix hasAgent: <http://semanticscience.org/resource/SIO_000139> .
@prefix species: <http://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?id=> .
@prefix occursIn: <http://purl.obolibrary.org/obo/BFO_0000066> .
@prefix mesh: <http://purl.bioontology.org/ontology/MSH/> .
@prefix pubmed: <http://www.ncbi.nlm.nih.gov/pubmed/> .
@prefix orcid: <http://orcid.org/> .

sub:Head {
  this: np:hasAssertion sub:assertion;
    np:hasProvenance sub:provenance;
    np:hasPublicationInfo sub:pubinfo;
    a np:Nanopublication .
}

sub:assertion {
  sub:_1 hasAgent: sub:_2;
    a go:0003824 .
  
  sub:_2 geneProductOf: hgnc:4706;
    a Protein: .
  
  sub:_3 occursIn: mesh:D017667, mesh:D018482, 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\") -> cat(p(HGNC:GYS1))" .
}

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:_5;
    pav:version "1.4" .
  
  sub:_4 prov:value "The ability of a variety of nutrients to activate the hexosamine pathway has led to the theory that this pathway serves as a general nutrient sensing pathway, through which hyperglycemia or hyperlipidemia could decrease insulin sensitivity of cells when nutrient excess prevails (148). In cell culture, omission of glutamine (a cofactor of GFA) from the media, or addition of glutamine analogues, blunts the desensitizing effect of glucose on insulin sensitivity (150). Glucosamine infusion for two to six hours will decrease insulin-stimulated IRS-1 tyrosine phosphorylation, PI3-kinase activation, and activation of glycogen synthase in a manner that parallels the decrease in insulin-stimulated glucose uptake in skeletal muscle. This effect can be seen both in acute and chronic stimulation with insulin (151) (Patti, M.E., personal communication).";
    prov:wasQuotedFrom pubmed:10194465 .
  
  sub:_5 rdfs:label "Selventa" .
  
  sub:assertion prov:hadPrimarySource pubmed:10194465;
    prov:wasDerivedFrom beldoc:, sub:_4 .
}

sub:pubinfo {
  this: dct:created "2014-07-03T14:29:46.653+02:00"^^xsd:dateTime;
    pav:createdBy orcid:0000-0001-6818-334X, orcid:0000-0002-1267-0234 .
}