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:_7 ;
    pav:version "20131211" .
  sub:_6 prov:value "In order to investigate the role of IRAK-4 kinase function in vivo, we generated \\\"knock-in\\\" mice where the wild-type IRAK-4 gene is replaced with a mutant gene encoding kinase-deficient IRAK-4 protein (IRAK-4 KD). IRAK-4 kinase is rendered inactive by mutating the conserved lysine residues in the ATP pocket essential for coordinating ATP. Analyses of embryonic fibroblasts and macrophages obtained from IRAK-4 KD mice demonstrated lack of cellular responsiveness to stimulation with IL-1beta or Toll-like receptor 4 (TLR4) and TLR7 agonists. IRAK-4 KD cells were severely impaired in NF-kappaB, JNK, and p38 activation in response to IL-1beta or TLR7 ligand." ;
    prov:wasQuotedFrom pubmed:18510099 .
  sub:_7 rdfs:label "Selventa" .
  sub:assertion prov:hadPrimarySource pubmed:18510099 ;
    prov:wasDerivedFrom beldoc: , sub:_6 .
}