@prefix this: <http://www.tkuhn.ch/bel2nanopub/RAuTsN4sph42QVDbm7jqGC7-tXRd0mH1AaMf_ftIhEyTs> .
@prefix sub: <http://www.tkuhn.ch/bel2nanopub/RAuTsN4sph42QVDbm7jqGC7-tXRd0mH1AaMf_ftIhEyTs#> .
@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 chebi: <http://www.ebi.ac.uk/chebi/searchId.do?chebiId=> .
@prefix mesh: <http://purl.bioontology.org/ontology/MSH/> .
@prefix species: <http://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?id=> .
@prefix occursIn: <http://purl.obolibrary.org/obo/BFO_0000066> .
@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 occursIn: species:9606;
    rdf:object mesh:D007333;
    rdf:predicate belv:increases;
    rdf:subject chebi:7242;
    a rdf:Statement .
  
  sub:assertion rdfs:label "a(CHEBI:ceramide) -> 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:_3;
    pav:version "1.4" .
  
  sub:_2 prov:value "In contrast, a PKB-PH domain with a T34A mutation retained the ability to bind PIP(3) even in the presence of a ceramide-activated PKCzeta and, as such, expression of PKB T34A mutant in L6 cells was resistant to inhibition by ceramide treatment. Inhibitors of PKCzeta and a kinase-dead PKCzeta both antagonized the inhibitory effect of ceramide on PKB. Since PKB confers a prosurvival signal and regulates numerous pathways in response to insulin, suppressing its activation by a PKCzeta-dependent process may be one mechanism by which ceramide promotes cell death and induces insulin resistance.";
    prov:wasQuotedFrom pubmed:14560023 .
  
  sub:_3 rdfs:label "Selventa" .
  
  sub:assertion prov:hadPrimarySource pubmed:14560023;
    prov:wasDerivedFrom beldoc:, sub:_2 .
}

sub:pubinfo {
  this: dct:created "2014-07-03T14:30:17.427+02:00"^^xsd:dateTime;
    pav:createdBy orcid:0000-0001-6818-334X, orcid:0000-0002-1267-0234 .
}