@prefix dct: .
@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 go: .
@prefix hasAgent: .
@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:11892;
a Protein: .
sub:_2 hasAgent: sub:_3;
a go:0042789 .
sub:_3 geneProductOf: hgnc:7794;
a Protein: .
sub:_4 occursIn: species:9606;
rdf:object sub:_2;
rdf:predicate belv:increases;
rdf:subject sub:_1;
a rdf:Statement .
sub:assertion rdfs:label "p(HGNC:TNF) -> tscript(p(HGNC:NFKB1))" .
}
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:_6;
pav:version "1.4" .
sub:_5 prov:value "This work presents direct evidence that the bcl-2 gene is transcriptionally regulated by nuclear factor-kappa B (NF-kappa B) and directly links the TNF-alpha/NF-kappa B signaling pathway with Bcl-2 expression and its pro-survival response in human prostate carcinoma cells. DNase I footprinting, gel retardation and supershift analysis identified a NF-kappa B site in the bcl-2 p2 promoter. In the context of a minimal promoter, this bcl-2 p2 site 1 increased transcription 10-fold in the presence of the p50/p65 expression vectors, comparable to the increment observed with the consensus NF-kappa B site, while for the full p2 promoter region transcriptional activity was increased sixfold by over-expression of NF-kappa B, an effect eliminated by mutating the bcl-2 p2 site 1. The expression of Bcl-2 has been linked to the hormone-resistant phenotype of advanced prostate cancer. Here we show that an increase in the level of expression of Bcl-2 in the human prostate carcinoma cell line LNCaP observed in response to hormone withdrawal is further augmented by TNF-alpha treatment, and this effect is abated by inhibitors of NF-kappa B. Concomitantly, bcl-2 p2 promoter studies in LNCaP cells show a 40-fold increase in promoter activity after stimulation with TNF-alpha in the absence of hormone.";
prov:wasQuotedFrom pubmed:11704864 .
sub:_6 rdfs:label "Selventa" .
sub:assertion prov:hadPrimarySource pubmed:11704864;
prov:wasDerivedFrom beldoc:, sub:_5 .
}
sub:pubinfo {
this: dct:created "2014-07-03T14:29:59.043+02:00"^^xsd:dateTime;
pav:createdBy orcid:0000-0001-6818-334X, orcid:0000-0002-1267-0234 .
}