@prefix this: <http://www.tkuhn.ch/bel2nanopub/RAP4DWrx5dduZejTy7A93rp9sJCXQmeLRPnLduxzmOq_s> .
@prefix sub: <http://www.tkuhn.ch/bel2nanopub/RAP4DWrx5dduZejTy7A93rp9sJCXQmeLRPnLduxzmOq_s#> .
@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 go: <http://amigo.geneontology.org/amigo/term/GO:> .
@prefix species: <http://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?id=> .
@prefix occursIn: <http://purl.obolibrary.org/obo/BFO_0000066> .
@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:10116;
    rdf:object go:0006954;
    rdf:predicate belv:increases;
    rdf:subject chebi:7583;
    a rdf:Statement .
  
  sub:assertion rdfs:label "a(CHEBI:\"nitric oxide\") -> bp(GO:\"inflammatory response\")" .
}

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:_2 dce:identifier "Cardiovascular Physiology Concepts";
    dce:title "Cardiovascular Physiology Concepts";
    dce:type "Other" .
  
  sub:_3 prov:value "Another important mechanism regulating the release of NO is shearing forces acting on the luminal surface of vascular endothelium.  By this mechanism, increased flow velocity stimulates calcium release and increased cNOS activity. The inducible form of NOS (iNOS, or Type II NOS) is not calcium-dependent, but instead is stimulated by the actions of cytokines (e.g., tumor necrosis factor, interleukins) and bacterial endotoxins (e.g., lipopolysaccharide).  Induction of iNOS occurs over several hours and results in NO production that may be more than a 1,000-fold greater than that produced by cNOS.  This is an important mechanism in the pathogenesis of inflammation.";
    prov:wasQuotedFrom sub:_2 .
  
  sub:_4 rdfs:label "Selventa" .
  
  sub:assertion prov:hadPrimarySource sub:_2;
    prov:wasDerivedFrom beldoc:, sub:_3 .
}

sub:pubinfo {
  this: dct:created "2014-07-03T14:29:45.331+02:00"^^xsd:dateTime;
    pav:createdBy orcid:0000-0001-6818-334X, orcid:0000-0002-1267-0234 .
}