@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 nch: . @prefix ProteinComplex: . @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 { nch:Nfkb%20Complex a ProteinComplex: . sub:_1 geneProductOf: hgnc:16; a Protein: . sub:_2 occursIn: species:9606; rdf:object sub:_1; rdf:predicate belv:increases; rdf:subject nch:Nfkb%20Complex; a rdf:Statement . sub:assertion rdfs:label "complex(NCH:\"Nfkb Complex\") -> p(HGNC:SERPINA3)" . } 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:_4; pav:version "1.4" . sub:_3 prov:value "The 5'-NF-KB high affinity binding site and AP-1 element contribute most to the enhancement of alpha1-antichymotrypsin gene transcription in response to TNF-alpha treatment. Mutation at 5'-NF-KB and AP-1 resulted in 60% and 50% reduction respectively, in responsiveness induced by TNF-alpha."; prov:wasQuotedFrom pubmed:11027208 . sub:_4 rdfs:label "Selventa" . sub:assertion prov:hadPrimarySource pubmed:11027208; prov:wasDerivedFrom beldoc:, sub:_3 . } sub:pubinfo { this: dct:created "2014-07-03T14:29:52.585+02:00"^^xsd:dateTime; pav:createdBy orcid:0000-0001-6818-334X, orcid:0000-0002-1267-0234 . }