@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 schem: . @prefix chebi: . @prefix atcc: . @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 { sub:_1 occursIn: atcc:HTB-22.aspx, species:9606; rdf:object chebi:23965; rdf:predicate belv:decreases; rdf:subject schem:Chlorinated%20dioxins; a rdf:Statement . sub:assertion rdfs:label "a(SCHEM:\"Chlorinated dioxins\") -| a(CHEBI:estradiol)" . } 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 "2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) and other aryl hydrocarbon receptor (AhR) ligands suppress 17beta-estradiol (E)-induced responses in the rodent uterus and mammary tumors and in human breast cancer cells. Treatment of ZR-75, T47D, and MCF-7 human breast cancer cells with TCDD induces proteasome-dependent degradation of endogenous estrogen receptor alpha (ERalpha)."; prov:wasQuotedFrom pubmed:12612060 . sub:_3 rdfs:label "Selventa" . sub:assertion prov:hadPrimarySource pubmed:12612060; prov:wasDerivedFrom beldoc:, sub:_2 . } sub:pubinfo { this: dct:created "2014-07-03T14:30:10.630+02:00"^^xsd:dateTime; pav:createdBy orcid:0000-0001-6818-334X, orcid:0000-0002-1267-0234 . }