@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 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:5992; a Protein: . sub:_2 geneProductOf: hgnc:9955; a Protein: . sub:_3 occursIn: species:9606; rdf:object sub:_2; rdf:predicate belv:increases; rdf:subject sub:_1; a rdf:Statement . sub:assertion rdfs:label "p(HGNC:IL1B) -> p(HGNC:RELA)" . } 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 "20131211" . sub:_4 prov:value "During hypoxia (3 h, 5% O2) in human neural (HN) cells combined treatment [IL-1 beta + amyloid beta peptide 42] increased AP-1, NFkappa B p65/p50, STAT1 alpha, and HIF-1 alpha-DNA binding by 3.3-, 6.5-, 4.8-, and 3.2-fold over normal controls. Hypoxia during aging contributed in Alzheimer's disease pathophysiology."; prov:wasQuotedFrom pubmed:12050157 . sub:_5 rdfs:label "Selventa" . sub:assertion prov:hadPrimarySource pubmed:12050157; prov:wasDerivedFrom beldoc:, sub:_4 . } sub:pubinfo { this: dct:created "2014-07-03T14:31:50.689+02:00"^^xsd:dateTime; pav:createdBy orcid:0000-0001-6818-334X, orcid:0000-0002-1267-0234 . }