@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 RNA: . @prefix hgnc: . @prefix geneProductOf: . @prefix species: . @prefix occursIn: . @prefix mesh: . @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:13633; a RNA: . sub:_2 occursIn: mesh:D017667, species:9606; rdf:object sub:_1; rdf:predicate belv:increases; rdf:subject chebi:50122; a rdf:Statement . sub:assertion rdfs:label "a(CHEBI:rosiglitazone) -> r(HGNC:ADIPOQ)" . } 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 "ZAG has recently been shown to be directly synthesized by white (and brown) adipocytes, there being a powerful upregulation at both the gene expression and protein levels in mice bearing the MAC16 tumour (a model for cachexia) (Bing et al. 2004). ZAG mRNA was increased 10-fold in the WAT of tumourbearing mice, while the level of leptin mRNA was reduced some 30-fold (Bing et al. 2004). In studies using human SGBS (Simpson-Golabi-Behmel syndrome) adipocytes, ZAG has now been shown to be released from fat cells, indicating that it is an adipokine (Bao et al. 2005). Expression of ZAG in human adipocytes is stimulated by the PPAR-c agonist rosiglitazone and suppressed by TNF-a, and this is similar to adiponectin (Bao et al. 2005)."; prov:wasQuotedFrom pubmed:16026420 . sub:_4 rdfs:label "Selventa" . sub:assertion prov:hadPrimarySource pubmed:16026420; prov:wasDerivedFrom beldoc:, sub:_3 . } sub:pubinfo { this: dct:created "2014-07-03T14:30:36.912+02:00"^^xsd:dateTime; pav:createdBy orcid:0000-0001-6818-334X, orcid:0000-0002-1267-0234 . }