@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 hgnc: . @prefix proteinModification: . @prefix psimod: . @prefix mesh: . @prefix obo: . @prefix occursIn: . @prefix species: . @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:12691; a proteinModification:, psimod:00696 . sub:_2 occursIn: obo:CL_0002518, species:9606; rdf:object mesh:D017209; rdf:predicate belv:decreases; rdf:subject sub:_1; a rdf:Statement . sub:assertion rdfs:label "p(HGNC:EZR,pmod(P,Y,353)) -| bp(MESHPP:Apoptosis)" . } 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 "20131211" . sub:_3 prov:value "Cells producing Y353F ezrin are defective in activation of the protein kinase Akt, a downstream target of PI 3-kinase that protects cells against apoptosis. Furthermore, the apoptotic phenotype of these cells is rescued by production of a constitutively activated form of PI 3-kinase. Taken together, these results establish a novel function for ezrin in determining survival of epithelial cells by activating the PI 3-kinase/Akt pathway."; prov:wasQuotedFrom pubmed:10377409 . sub:_4 rdfs:label "Selventa" . sub:assertion prov:hadPrimarySource pubmed:10377409; prov:wasDerivedFrom beldoc:, sub:_3 . } sub:pubinfo { this: dct:created "2014-07-03T14:31:30.852+02:00"^^xsd:dateTime; pav:createdBy orcid:0000-0001-6818-334X, orcid:0000-0002-1267-0234 . }