@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 RNA: .
@prefix mgi: .
@prefix geneProductOf: .
@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:96693;
a RNA: .
sub:_2 occursIn: species:10090;
rdf:object sub:_1;
rdf:predicate belv:increases;
rdf:subject chebi:23965;
a rdf:Statement .
sub:assertion rdfs:label "a(CHEBI:estradiol) -> r(MGI:Krt19)" .
}
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 "20131211" .
sub:_3 prov:value "Stimulation by estradiol (E2) of K19 mRNA is rapid, with maximal increase at 3 h, and is not blocked by cycloheximide, suggesting that it is a primary response to the hormone. Increased accumulation of K19 protein is observable by 8 h after E2 and levels continue to increase at 24-48 h after E2 treatment. Suppression of E2-induced K19 gene expression by the antiestrogen ICI 182,780 suggests that ER mediates this regulation.";
prov:wasQuotedFrom pubmed:11026574 .
sub:_4 rdfs:label "Selventa" .
sub:assertion prov:hadPrimarySource pubmed:11026574;
prov:wasDerivedFrom beldoc:, sub:_3 .
}
sub:pubinfo {
this: dcterms:created "2014-07-03T14:31:37.434+02:00"^^xsd:dateTime;
pav:createdBy orcid:0000-0001-6818-334X, orcid:0000-0002-1267-0234 .
}