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Updated: Aug 3, 2026

Structure-function Studies in Mouse Embryonic Stem Cells Using Recombinase-mediated Cassette Exchange
Published on: April 27, 2017
The ectodermal dysplasia receptor represses the Lef-1/beta-catenin-dependent transcription independent of NF-kappaB
Masahisa Shindo1, Preet M Chaudhary
1The Hamon Center for Therapeutic Oncology Research and Division of Hematology-Oncology, UT Southwestern Medical Center, Dallas, TX 75390-8593, USA.
Abstract:
EDAR plays a key role in the process of ectodermal differentiation via activation of the NF-kappaB pathway. We present evidence that EDAR also represses Lef-1/beta-catenin-dependent transcription and this ability is defective in EDAR mutants associated with anhidrotic ectodermal dysplasia. While IKK1/IKKalpha and IKK2/IKKbeta are required for EDAR-induced NF-kappaB activation, they are dispensable for its ability to repress Lef-1/beta-catenin-dependent transcription. In contrast, NIK is not involved in EDAR-induced NF-kappaB activation or Lef-1/beta-catenin transcriptional repression. As Lef-1/beta-catenin pathway controls the expression of EDAR ligand, ectodysplasin-A (EDA), our results point to a negative feedback regulation of EDA-EDAR axis.
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