@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 mesh: . @prefix hgnc: . @prefix proteinModification: . @prefix psimod: . @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 { sub:_1 belv:variantOf hgnc:3214; a proteinModification:, psimod:00696 . sub:_2 occursIn: species:9606; rdf:object sub:_1; rdf:predicate belv:decreases; rdf:subject mesh:D015444; a rdf:Statement . sub:assertion rdfs:label "bp(MESHPP:Exercise) -| p(HGNC:EEF2,pmod(P))" . } 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 "increasing the workload resulted in a dephosphorylation of eEF2, which was rapamycin-insensitive, thus excluding a role for mTOR in this effect. eEF2K activity was unchanged by increasing the workload, suggesting that the decrease in eEF2 phosphorylation could result from the activation of an eEF2 phosphatase."; prov:wasQuotedFrom pubmed:12920134 . sub:_4 rdfs:label "Selventa" . sub:assertion prov:hadPrimarySource pubmed:12920134; prov:wasDerivedFrom beldoc:, sub:_3 . } sub:pubinfo { this: dct:created "2014-07-03T14:30:15.569+02:00"^^xsd:dateTime; pav:createdBy orcid:0000-0001-6818-334X, orcid:0000-0002-1267-0234 . }