@prefix dcterms: .
@prefix this: .
@prefix sub: .
@prefix beldoc: .
@prefix rdfs: .
@prefix rdf: .
@prefix xsd: .
@prefix dce: .
@prefix pav: .
@prefix np: .
@prefix belv: .
@prefix prov: .
@prefix chebi: .
@prefix Protein: .
@prefix rgd: .
@prefix geneProductOf: .
@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 geneProductOf: rgd:2741;
a Protein: .
sub:_2 occursIn: mesh:D008099, species:10116;
rdf:object sub:_1;
rdf:predicate belv:decreases;
rdf:subject chebi:6934;
a rdf:Statement .
sub:assertion rdfs:label "a(CHEBI:mifepristone) -| p(RGD:Nr3c1)" .
}
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 "When hepatocytes were co-incubated with DEX and antiglucocorticoid/antiprogestin RU-486, DEX-stimulated HST-a mRNA expression was not significantly inhibited by RU-486, but ASTIV and TAT mRNA expression were inhibited to a similar extent. The results suggested that ASTIV, like TAT, is likely regulated by a classical glucocorticoid receptor mediated mechanism, whereas HST-a is probably regulated by glucocorticoids via an alternative mechanism.";
prov:wasQuotedFrom pubmed:9566755 .
sub:_4 rdfs:label "Selventa" .
sub:assertion prov:hadPrimarySource pubmed:9566755;
prov:wasDerivedFrom beldoc:, sub:_3 .
}
sub:pubinfo {
this: dcterms:created "2014-07-03T14:30:59.698+02:00"^^xsd:dateTime;
pav:createdBy orcid:0000-0001-6818-334X, orcid:0000-0002-1267-0234 .
}