@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 chebi: . @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:0003824 . sub:_2 geneProductOf: hgnc:2577; a Protein: . sub:_3 occursIn: species:9606; rdf:object sub:_1; rdf:predicate belv:increases; rdf:subject chebi:26523; a rdf:Statement . sub:assertion rdfs:label "a(CHEBI:\"reactive oxygen species\") -> cat(p(HGNC:CYBA))" . } 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 "# GeneRif: These findings suggest a positive feedback mechanism whereby reactive oxygen species (ROS), possibly generated by the NADPH oxidase, lead to elevated levels of p22phox and, thus, sustained ROS generation as is observed in endothelial dysfunction."; prov:wasQuotedFrom pubmed:15683718 . sub:_5 rdfs:label "Selventa" . sub:assertion prov:hadPrimarySource pubmed:15683718; prov:wasDerivedFrom beldoc:, sub:_4 . } sub:pubinfo { this: dct:created "2014-07-03T14:30:31.306+02:00"^^xsd:dateTime; pav:createdBy orcid:0000-0001-6818-334X, orcid:0000-0002-1267-0234 . }