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 "20131211" .
  sub:_4 prov:value "Rosiglitazone has marked anti-inflammatory effects on macrophages [31]. This led us to examine the effect of aspirin, an anti-inflammatory compound that targets IkB kinase and has insulin-sensitizing effects [32]. Remarkably, aspirin dramatically decreased endotoxin-induced resistin expression in a dose-dependent manner (Figure 4C). Both aspirin (via IkB kinase) and rosiglitazone (via PPARg) inhibit NF-kB [31,32], which is activated by LPS. Indeed, treatment of the macrophages with the proteasome inhibitor MG132, which prevents NF-kB activation [33], abrogated endotoxin-induced activation of resistin expression (data not shown). Moreover, treatment of the macrophages with SN50, a cell-permeable peptide that specifically prevents activation of NF-kB by inhibiting its nuclear translocation [34], nearly abolished endotoxin-induced activation of resistin expression (Figure 4D). Thus, activation of NF-kB is required for LPS induction of resistin in human macrophages." ;
    prov:wasQuotedFrom pubmed:15578112 .
  sub:_5 rdfs:label "Selventa" .
  sub:assertion prov:hadPrimarySource pubmed:15578112 ;
    prov:wasDerivedFrom beldoc: , sub:_4 .
}