@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 microRNA: .
@prefix hgnc: .
@prefix geneProductOf: .
@prefix RNA: .
@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: hgnc:31586;
a microRNA: .
sub:_2 geneProductOf: hgnc:8763;
a RNA: .
sub:_3 occursIn: species:9606;
rdf:object sub:_2;
rdf:predicate belv:decreases;
rdf:subject sub:_1;
a rdf:Statement .
sub:assertion rdfs:label "m(HGNC:MIR21) -| r(HGNC:PDCD4)" .
}
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 "nhibitors of miR-21 increased protein levels of programmed cell death 4 (PDCD4) and tissue inhibitor of metalloproteinases 3 (TIMP3). Notably, messenger RNA levels of TIMP3 were significantly lower in CCAs than in normals. Conclusions: MiR-21 is overexpressed in human CCAs. Furthermore, miR-21 may be oncogenic, at least in part, by inhibiting PDCD4 and TIMP3";
prov:wasQuotedFrom pubmed:19296468 .
sub:_5 rdfs:label "Selventa" .
sub:assertion prov:hadPrimarySource pubmed:19296468;
prov:wasDerivedFrom beldoc:, sub:_4 .
}
sub:pubinfo {
this: dcterms:created "2014-07-03T14:30:54.722+02:00"^^xsd:dateTime;
pav:createdBy orcid:0000-0001-6818-334X, orcid:0000-0002-1267-0234 .
}