@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 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:5464;
a Protein: .
sub:_2 hasAgent: sub:_3;
a go:0042789 .
sub:_3 geneProductOf: hgnc:6769;
a Protein: .
sub:_4 occursIn: species:9606;
rdf:object sub:_2;
rdf:predicate belv:decreases;
rdf:subject sub:_1;
a rdf:Statement .
sub:assertion rdfs:label "p(HGNC:IGF1) -| tscript(p(HGNC:SMAD3))" .
}
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 "The phosphatidylinositol 3-kinase (PI3K) inhibitor, LY29004 reverses the ability of IGF-I to inhibit TGF-beta-induced transcriptional responses and the activation of Smad3, suggesting that the suppression of TGF-beta signaling by IGF-I is mediated through activation of PI3K. Moreover, we show that enforced expression of dominant-negative PI3K (DN-p85alpha) or phosphatidylinositol 3-phosphate-phosphatase, PTEN, also reverse the suppressive effect of IGF-I on TGF-beta-induced 3TP-luciferase reporter activity, whereas constitutively active PI3K (p110alphaCAAX) completely blocks TGF-beta-induced 3TP-luciferase reporter activity.";
prov:wasQuotedFrom pubmed:12876289 .
sub:_6 rdfs:label "Selventa" .
sub:assertion prov:hadPrimarySource pubmed:12876289;
prov:wasDerivedFrom beldoc:, sub:_5 .
}
sub:pubinfo {
this: dcterms:created "2014-07-03T14:30:14.886+02:00"^^xsd:dateTime;
pav:createdBy orcid:0000-0001-6818-334X, orcid:0000-0002-1267-0234 .
}