Molecular basis of hypohidrotic ectodermal dysplasia: an update

J Appl Genet. 2016 Feb;57(1):51-61. doi: 10.1007/s13353-015-0307-4. Epub 2015 Aug 21.

Abstract

Recent advances in understanding the molecular events underlying hypohidrotic ectodermal dysplasia (HED) caused by mutations of the genes encoding proteins of the tumor necrosis factor α (TNFα)-related signaling pathway have been presented. These proteins are involved in signal transduction from ectoderm to mesenchyme during development of the fetus and are indispensable for the differentiation of ectoderm-derived structures such as eccrine sweat glands, teeth, hair, skin, and/or nails. Novel data were reviewed and discussed on the structure and functions of the components of TNFα-related signaling pathway, the consequences of mutations of the genes encoding these proteins, and the prospect for further investigations, which might elucidate the origin of HED.

Keywords: Differentiation of skin appendages; Hypohidrotic ectodermal dysplasia; TNFα-related signaling pathway.

Publication types

  • Review

MeSH terms

  • Ectoderm / growth & development
  • Ectodermal Dysplasia / genetics*
  • Ectodermal Dysplasia / therapy
  • Humans
  • Inheritance Patterns
  • Mesoderm / growth & development
  • Mutation
  • NF-kappa B / genetics
  • Signal Transduction / genetics*
  • Tumor Necrosis Factor-alpha / genetics*

Substances

  • NF-kappa B
  • Tumor Necrosis Factor-alpha