@prefix this: <http://www.tkuhn.ch/bel2nanopub/RAaA9PzEp5rmSWN04wh5ByESwKyCayh64bNJJWsC44Oqc> .
@prefix sub: <http://www.tkuhn.ch/bel2nanopub/RAaA9PzEp5rmSWN04wh5ByESwKyCayh64bNJJWsC44Oqc#> .
@prefix beldoc: <http://resource.belframework.org/belframework/1.0/knowledge/large_corpus.bel> .
@prefix rdfs: <http://www.w3.org/2000/01/rdf-schema#> .
@prefix rdf: <http://www.w3.org/1999/02/22-rdf-syntax-ns#> .
@prefix xsd: <http://www.w3.org/2001/XMLSchema#> .
@prefix dct: <http://purl.org/dc/terms/> .
@prefix dce: <http://purl.org/dc/elements/1.1/> .
@prefix pav: <http://purl.org/pav/> .
@prefix np: <http://www.nanopub.org/nschema#> .
@prefix belv: <http://www.selventa.com/vocabulary/> .
@prefix prov: <http://www.w3.org/ns/prov#> .
@prefix Protein: <http://www.ebi.ac.uk/chebi/searchId.do?chebiId=CHEBI_36080> .
@prefix hgnc: <http://www.genenames.org/cgi-bin/gene_symbol_report?hgnc_id=> .
@prefix geneProductOf: <http://purl.obolibrary.org/obo/RO_0002204> .
@prefix mesh: <http://purl.bioontology.org/ontology/MSH/> .
@prefix species: <http://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?id=> .
@prefix occursIn: <http://purl.obolibrary.org/obo/BFO_0000066> .
@prefix pubmed: <http://www.ncbi.nlm.nih.gov/pubmed/> .
@prefix orcid: <http://orcid.org/> .

sub:Head {
  this: np:hasAssertion sub:assertion;
    np:hasProvenance sub:provenance;
    np:hasPublicationInfo sub:pubinfo;
    a np:Nanopublication .
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sub:assertion {
  sub:_1 geneProductOf: hgnc:17712;
    a Protein: .
  
  sub:_2 occursIn: species:9606;
    rdf:object mesh:D017209;
    rdf:predicate belv:increases;
    rdf:subject sub:_1;
    a rdf:Statement .
  
  sub:assertion rdfs:label "p(HGNC:SIVA1) -> bp(MESHPP:Apoptosis)" .
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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 "In contrast to Bid, the antiapoptotic members of the Bcl-2 protein family, such as Bcl-2 and Bcl-xL, are known to preserve the integrity of the mitochondrial membrane (34). We thus explored whether the Siva-induced apoptosis in T cells could be modulated by overexpression of Bcl-2 or Bcl-xL. Jurkat T cells overexpressing either Bcl-2 or Bcl-xL were transiently transfected with the GFP-Siva-1 expression vector, and cell surface PS exposure was analyzed 48 h later on GFP-positive cells (Fig. 5C). Expression of GFP-Siva-1 in control Jurkat cells stably transfected with the neomycin vector resulted in an apoptotic level absolutely similar to that observed in HPB-ALL T cells. In contrast, the percentage of GFP-Siva-1-expressing cells displaying a cell surface exposure of PS was reduced to a level corresponding to the GFP control in cells coexpressing Bcl-2 or Bcl-xL. These results show that the proapoptotic activity of GFP-Siva-1 in Jurkat T cells can be totally abrogated by overexpression of either Bcl-2 or Bcl-xL antiapoptotic proteins. Because studies on the Fas-mediated apoptosis signaling pathways have highlighted two types of cells (35) depending on the requirement (type II cells such as Jurkat cells) or not (type I cells) of a mitochondrial amplification loop, we explored the Siva-induced apoptosis in a type I cell line such as SKW6.4 B lymphoid cells overexpressing Bcl-2 (35). In contrast to Jurkat cells, overexpression of Bcl-2 in SKW6.4 cells only reduced by 50% the proportion of apoptotic GFP-Siva-1-expressing cells (Fig. 5D). This result indicates that the Siva-induced apoptosis is also, at least in part, modulated by antiapoptotic members of the Bcl-2 protein family in type I cells. (From full text)";
    prov:wasQuotedFrom pubmed:15034012 .
  
  sub:_4 rdfs:label "Selventa" .
  
  sub:assertion prov:hadPrimarySource pubmed:15034012;
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sub:pubinfo {
  this: dct:created "2014-07-03T14:30:21.718+02:00"^^xsd:dateTime;
    pav:createdBy orcid:0000-0001-6818-334X, orcid:0000-0002-1267-0234 .
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