@prefix this: . @prefix sub: . @prefix beldoc: . @prefix rdfs: . @prefix rdf: . @prefix xsd: . @prefix dct: . @prefix dce: . @prefix pav: . @prefix np: . @prefix belv: . @prefix prov: . @prefix Protein: . @prefix hgnc: . @prefix geneProductOf: . @prefix mesh: . @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:5472; a Protein: . sub:_2 occursIn: species:9606; rdf:object mesh:D017209; rdf:predicate belv:increases; rdf:subject sub:_1; a rdf:Statement . sub:assertion rdfs:label "p(HGNC:IGFBP3) -> bp(MESHPP:Apoptosis)" . } 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 "1.4" . sub:_3 prov:value "Among these targets, the insulin-like growth factor binding protein 3 gene (IGFBP-3), a major regulator of insulin-like growth factor 1 (IGF-1) proliferation and survival signaling, was strongly induced upon treating Ewing cells with EWS/FLI-1-specific small interfering RNAs. We show that EWS/FLI-1 can bind the IGFBP-3 promoter in vitro and in vivo and can repress its activity. Moreover, IGFBP-3 silencing can partially rescue the apoptotic phenotype caused by EWS/FLI-1 inactivation."; prov:wasQuotedFrom pubmed:15282325 . sub:_4 rdfs:label "Selventa" . sub:assertion prov:hadPrimarySource pubmed:15282325; prov:wasDerivedFrom beldoc:, sub:_3 . } sub:pubinfo { this: dct:created "2014-07-03T14:30:26.176+02:00"^^xsd:dateTime; pav:createdBy orcid:0000-0001-6818-334X, orcid:0000-0002-1267-0234 . }