@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 ncm: . @prefix ProteinComplex: . @prefix mesh: . @prefix occursIn: . @prefix species: . @prefix pubmed: . @prefix orcid: . sub:Head { this: np:hasAssertion sub:assertion; np:hasProvenance sub:provenance; np:hasPublicationInfo sub:pubinfo; a np:Nanopublication . } sub:assertion { ncm:Nfkb%20Complex a ProteinComplex: . sub:_1 occursIn: mesh:D008264, species:10090; rdf:object mesh:D050197; rdf:predicate belv:decreases; rdf:subject ncm:Nfkb%20Complex; a rdf:Statement . sub:assertion rdfs:label "complex(NCM:\"Nfkb Complex\") -| path(MESHD:Atherosclerosis)" . } 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:_3; pav:version "1.4" . sub:_2 prov:value "To investigate the role of NF-kappaB activation in macrophages during atherogenesis, we used LDL receptor-deficient mice with a macrophage-restricted deletion of IkappaB kinase 2 (IKK2), which is essential for NF-kappaB activation by proinflammatory signals. These mice showed increased atherosclerosis as quantified by lesion area measurements."; prov:wasQuotedFrom pubmed:14561702 . sub:_3 rdfs:label "Selventa" . sub:assertion prov:hadPrimarySource pubmed:14561702; prov:wasDerivedFrom beldoc:, sub:_2 . } sub:pubinfo { this: dct:created "2014-07-03T14:30:17.443+02:00"^^xsd:dateTime; pav:createdBy orcid:0000-0001-6818-334X, orcid:0000-0002-1267-0234 . }