@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 go: . @prefix Protein: . @prefix mgi: . @prefix geneProductOf: . @prefix hasAgent: . @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 hasAgent: sub:_2; a go:0042789 . sub:_2 geneProductOf: mgi:94902; a Protein: . sub:_3 geneProductOf: mgi:1097716; a RNA: . sub:_4 occursIn: species:10090; rdf:object sub:_3; rdf:predicate belv:directlyIncreases; rdf:subject sub:_1; a rdf:Statement . sub:assertion rdfs:label "tscript(p(MGI:Dlx2)) => r(MGI:Arx)" . } 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 "20131211" . sub:_5 prov:value "Functional characterization of the Arx GABAergic enhancer element revealed its strict dependence on the activity of Dlx transcription factors. Dlx overexpression induces ectopic expression of endogenous Arx and its isolated enhancer, whereas loss of Dlx expression results in reduced Arx expression, suggesting that Arx is a key mediator of Dlx function.....Arx is a direct target of Dlx2 "; prov:wasQuotedFrom pubmed:18923043 . sub:_6 rdfs:label "Selventa" . sub:assertion prov:hadPrimarySource pubmed:18923043; prov:wasDerivedFrom beldoc:, sub:_5 . } sub:pubinfo { this: dct:created "2014-07-03T14:33:26.545+02:00"^^xsd:dateTime; pav:createdBy orcid:0000-0001-6818-334X, orcid:0000-0002-1267-0234 . }