sub:provenance {
  beldoc: dce:description "Approximately 2000 hand curated statements drawn from 57 PubMeds." ;
    dce:rights "Copyright (c) 2011-2012, Selventa. All Rights Reserved." ;
    dce:title "BEL Framework Small Corpus Document" ;
    dc:license "Creative Commons Attribution-Non-Commercial-ShareAlike 3.0 Unported License" ;
    pav:authoredBy sub:_8 ;
    pav:version "1.6" .
  sub:_7 prov:value """However, IL-1β-induced NF-κB activity is attenuated by increased intracellular calcium
in response to ionomycin, UTP, or thapsigargin or by overexpression of CaMKKc
and/or Akt. Ionomycin and CaMKKc overexpression increases Akt phosphorylation
on Thr308 and enzyme activity. Under these conditions or upon overexpression of
wild type Akt, IL-1β-induced IKKβ activity is diminished. Furthermore, a dominant
negative mutant of Akt abolishes IKKβ inhibition by CaMKKc and ionomycin, suggesting
that Akt acts as a mediator of CaMKK signaling to inhibit IL-1β-induced
IKK activity at an upstream target site.""" ;
    prov:wasQuotedFrom pubmed:11976320 .
  sub:_8 rdfs:comment "support@belframework.org" ;
    rdfs:label "Selventa" .
  sub:assertion prov:hadPrimarySource pubmed:11976320 ;
    prov:wasDerivedFrom beldoc: , sub:_7 .
}