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:_6 ;
    pav:version "1.4" .
  sub:_5 prov:value "Jung et al. [36] recently investigated TNF-a-induced HIF-1a accumulation and demonstrated that an NFkB-mediated event that is normally associated with inflammation and cell survival caused protein accumulation in normoxic cells. Although the report fails to identify the mechanism of HIF-1a accumulation, it is suggested that this might interfere with the pVHL-mediated HIF-1a degradation process. Further studies support the concept of a pVHL-dependent cytotoxicity to TNF-a in RCC cells [37,38]. In particular, it has been reported that RCC cells can be sensitized to TNF-a-induced cytotoxicity by re-introducing wild-type VHL [38]. The authors highlight the fact that TNFreceptor engagement by TNF-a triggers the activation of atypical protein kinase C (aPKC), which, through IKKb phosphorylation, liberates NFkB, thereby initiating the transcription of genes that are involved in apoptosis." ;
    prov:wasQuotedFrom pubmed:15350900 .
  sub:_6 rdfs:label "Selventa" .
  sub:assertion prov:hadPrimarySource pubmed:15350900 ;
    prov:wasDerivedFrom beldoc: , sub:_5 .
}