@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 hgnc: . @prefix geneProductOf: . @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 hasAgent: sub:_2; a go:0042789 . sub:_2 geneProductOf: hgnc:785; a Protein: . sub:_3 occursIn: species:9606; rdf:object go:0008283; rdf:predicate belv:increases; rdf:subject sub:_1; a rdf:Statement . sub:assertion rdfs:label "tscript(p(HGNC:ATF3)) -> bp(GO:\"cell proliferation\")" . } 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 "The results showed that only ATF3 had a strong interaction with Restin. It is interesting to know that ATF3 was an important transcription factor for G1 cell cycle initiation in physiological stress response. It was possible that the inhibition of cell proliferation by Restin might be related with the inhibition of ATF3 activity."; prov:wasQuotedFrom pubmed:16092758 . sub:_5 rdfs:label "Selventa" . sub:assertion prov:hadPrimarySource pubmed:16092758; prov:wasDerivedFrom beldoc:, sub:_4 . } sub:pubinfo { this: dct:created "2014-07-03T14:30:37.498+02:00"^^xsd:dateTime; pav:createdBy orcid:0000-0001-6818-334X, orcid:0000-0002-1267-0234 . }