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 "20131211" .
  sub:_5 prov:value "overexpression of HIPK2 suppresses LEF1/beta-catenin-mediated transcriptional activation of cyclin D1 expression. Our results indicated that HIPK2 suppressed ?-catenin-mediated activation of cyclin D1 (Fig. 3F). The suppressive effect of HIPK2 did not require phosphorylation on the critical Ser/Thr residues of ?-catenin because HIPK2 suppressed the transcriptional activity of a constitutively active form of ?-catenin (CA-?-catenin) in which amino acids 29–48 were deleted (Fig. 3F). Interestingly, the kinase-inactive form of HIPK2 (HIPK2K221A) showed a similar efficacy in suppressing cyclin D1 expression, suggesting that the kinase activity of HIPK2 was dispensable. " ;
    prov:wasQuotedFrom pubmed:17666529 .
  sub:_6 rdfs:label "Selventa" .
  sub:assertion prov:hadPrimarySource pubmed:17666529 ;
    prov:wasDerivedFrom beldoc: , sub:_5 .
}