@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 species: . @prefix occursIn: . @prefix obo: . @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: obo:CL_0000169, obo:EFO_0002795, obo:UBERON_0001986, species:9606; rdf:object chebi:26523; rdf:predicate belv:increases; rdf:subject schem:serum%20leptin; a rdf:Statement . sub:assertion rdfs:label "a(SCHEM:\"serum leptin\") -> a(CHEBI:\"reactive oxygen species\")" . } 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 "20131211" . sub:_2 prov:value "Normal leptin receptor, but not the mutated form present in fa/fa rats, has been shown to lead to changes in PDE2 expression and activity in brown fat [99]. Therefore, regulation of PDE isoforms by leptin is apparent in various tissues and further work will help understand the mechanism and consequences of this action. There are several other signalling proteins regulated by leptin that should be mentioned here. Two studies have demonstrated an ability of leptin to increase production of reactive oxygen species (ROS) in human umbilical vein endothelial cells (HUVEC) or bovine aortic endothelial cells (BAEC) [65,119]."; prov:wasQuotedFrom pubmed:12020765 . sub:_3 rdfs:label "Selventa" . sub:assertion prov:hadPrimarySource pubmed:12020765; prov:wasDerivedFrom beldoc:, sub:_2 . } sub:pubinfo { this: dct:created "2014-07-03T14:31:49.247+02:00"^^xsd:dateTime; pav:createdBy orcid:0000-0001-6818-334X, orcid:0000-0002-1267-0234 . }