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:_4 ;
    pav:version "20131211" .
  sub:_3 prov:value "To determine whether activation of the Wnt pathway directly up-regulates the VEGF promoter, an oncogenic ß-cateninS37A was transfected with the 2.8-kb VEGF-pGL2 reporter into HeLa cells. A critical serine phosphorylation site at amino acid 37 that ordinarily targets ß-catenin for degradation has been mutated (10) . Fig. 1D.  Citation  illustrates a linear dose response to the effects of ß-cateninS37A. The peak response was observed when 1.25 µg of expression vector was cotransfected with 0.75 µg of reporter vector, resulting in a >30-fold stimulation of VEGF promoter activity. In independent studies, HeLa cells were treated with 25 mM LiCl, an inhibitor of GSK-3ß kinase activity. GSK-3ß is a negative regulator of Wnt signaling, and inhibiting GSK-3ß with LiCl resulted in a 2.2-fold increase in VEGF promoter activity. Collectively, these findings indicate that activation of Wnt signaling up-regulates VEGF expression in colonic neoplasia. (from full text) " ;
    prov:wasQuotedFrom pubmed:11507052 .
  sub:_4 rdfs:label "Selventa" .
  sub:assertion prov:hadPrimarySource pubmed:11507052 ;
    prov:wasDerivedFrom beldoc: , sub:_3 .
}