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 "1.4" .
  sub:_5 prov:value "MITF in the commitment, proliferation, and survival of melanocytes before and/or during neural crest cell migration beta-catenin, a multifunctional protein which can either bind to E-cadherins as an integral part of the actin cytoskeleton which anchors cell cell adhesion, or can act as a transcriptional coactivator by interacting with the T-cell transcription factor (TCF)/lymphoid enhancer binding factor (LEF) family of DNA binding proteins in the nucleus. In the absence of Wnt-signals, beta-catenin is targeted for degradation via phosphorylation by a complex consisting of glycogen synthase kinase (GSK)3beta, axin, and adenomatous polyposis coli protein (APC). Wnt signals lead to inactivation of GSK3beta, and thus stabilize beta-catenin levels in the cell which increase transcription of downstream target genes. In human melanoma, stabilizing mutations of beta-catenin have been found in a significant fraction of established cell lines. Importantly, in primary human melanoma specimens, almost one third display aberrant nuclear accumulation of beta-catenin, although generally without evidence of direct mutations within the beta-catenin gene itself In mammalian cells, Wnt-3a, was also shown to induce MITF expression" ;
    prov:wasQuotedFrom pubmed:12235125 .
  sub:_6 rdfs:label "Selventa" .
  sub:assertion prov:hadPrimarySource pubmed:12235125 ;
    prov:wasDerivedFrom beldoc: , sub:_5 .
}