@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 Protein: .
@prefix hgnc: .
@prefix geneProductOf: .
@prefix mesh: .
@prefix occursIn: .
@prefix species: .
@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:5992;
a Protein: .
sub:_2 geneProductOf: hgnc:5986;
a Protein: .
sub:_3 occursIn: mesh:D005347, species:9606;
rdf:object sub:_2;
rdf:predicate belv:increases;
rdf:subject sub:_1;
a rdf:Statement .
sub:assertion rdfs:label "p(HGNC:IL1B) -> p(HGNC:IL18)" .
}
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 "Besides its direct angiogenic role, other potential mechanisms of the angiogenic function of IL-18 may be through IL-8 and other angiogenic cytokines that it up-regulates. Indeed, IL-18 exerts an inflammatory cytokine cascade in the mixed PBMC population by stimulating the constitutive expression of IL-18R on NK cells and lymphocytes, which leads to TNF-a production, ultimately stimulating macrophage IL-1b and IL-8 production (19). In turn, treatment with IL-1b and TNF-a of RA synovial fibroblast cultures, not constitutively expressing IL-18, induced IL-18 gene and protein production, suggesting a feedback interaction to promote Th1 cytokine and cell development in RA (21).";
prov:wasQuotedFrom pubmed:11466388 .
sub:_5 rdfs:label "Selventa" .
sub:assertion prov:hadPrimarySource pubmed:11466388;
prov:wasDerivedFrom beldoc:, sub:_4 .
}
sub:pubinfo {
this: dcterms:created "2014-07-03T14:29:57.517+02:00"^^xsd:dateTime;
pav:createdBy orcid:0000-0001-6818-334X, orcid:0000-0002-1267-0234 .
}