@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 mesh: . @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 occursIn: species:9606; rdf:object mesh:D053938; rdf:predicate belv:increases; rdf:subject chebi:9252; a rdf:Statement . sub:assertion rdfs:label "a(CHEBI:staurosporine) -> bp(MESHPP:\"DNA Fragmentation\")" . } 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 "Non-small-cell lung carcinomas (NSCLCs) are resistant to the induction of apoptosis by conventional anticancer treatment. However, NSCLC cell lines are sensitive to the action of the broad protein kinase inhibitor, staurosporine (STS). In the NSCLC cell line U1810, STS induced the mitochondrial release of apoptosis-inducing factor (AIF) and cytochrome c (Cyt c) followed by activation of caspases, nuclear condensation, DNA fragmentation and finally cell death."; prov:wasQuotedFrom pubmed:15286713 . sub:_3 rdfs:label "Selventa" . sub:assertion prov:hadPrimarySource pubmed:15286713; prov:wasDerivedFrom beldoc:, sub:_2 . } sub:pubinfo { this: dct:created "2014-07-03T14:30:26.228+02:00"^^xsd:dateTime; pav:createdBy orcid:0000-0001-6818-334X, orcid:0000-0002-1267-0234 . }