. . . . . . . . . . . . . . . "tscript(p(PFH:\"TCF/LEF Family\")) -> r(HGNC:MITF)" . "Approximately 61,000 statements." . "Copyright (c) 2011-2012, Selventa. All rights reserved." . "BEL Framework Large Corpus Document" . . "1.4" . "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" . . "Selventa" . . . . "2014-07-03T14:30:05.958+02:00"^^ . . .