@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 go: . @prefix Protein: . @prefix mgi: . @prefix geneProductOf: . @prefix hasAgent: . @prefix sdis: . @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 hasAgent: sub:_2; a go:0016301 . sub:_2 geneProductOf: mgi:1346865; a Protein: . sub:_3 occursIn: mesh:D018482, species:10090; rdf:object sdis:tumor%20growth; rdf:predicate belv:decreases; rdf:subject sub:_1; a rdf:Statement . sub:assertion rdfs:label "kin(p(MGI:Mapk14)) -| path(SDIS:\"tumor growth\")" . } 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:_5; pav:version "1.4" . sub:_4 prov:value "Both dominant-negative and chemical reagents were used to establish the finding that p38 MAPK signaling can trigger cell senescence. One report systematically showed that p38 MAPK activity was responsible for executing senescence in response to all the known stimuli telomere shortening, H2O2 exposure, and chronic RAS oncogene signaling (Haq et al., 2002; Wang et al., 2002 and Iwasa et al., 2003). When considered together, several papers also suggest that p38 MAPK activation is linked to tumor suppression (Bulavin et al., 2002; Pruitt et al., 2002; Brancho et al., 2003 and Liao and Hung, 2003)."; prov:wasQuotedFrom pubmed:15225871 . sub:_5 rdfs:label "Selventa" . sub:assertion prov:hadPrimarySource pubmed:15225871; prov:wasDerivedFrom beldoc:, sub:_4 . } sub:pubinfo { this: dct:created "2014-07-03T14:30:25.336+02:00"^^xsd:dateTime; pav:createdBy orcid:0000-0001-6818-334X, orcid:0000-0002-1267-0234 . }