| Literature DB >> 27838789 |
Hanan E Shamseldin1, Ola Khalifa2,3, Yousef M Binamer4, Abdulmonem Almutawa5, Stefan T Arold6, Hamad Zaidan7, Fowzan S Alkuraya8,9.
Abstract
Ectodermal dysplasia is a highly heterogeneous group of disorders that variably affect the derivatives of the ectoderm, primarily skin, hair, nails and teeth. TP63, itself mutated in ectodermal dysplasia, links many other ectodermal dysplasia disease genes through a regulatory network that maintains the balance between proliferation and differentiation of the epidermis and other ectodermal derivatives. The ectodermal knockout phenotype of five mouse genes that regulate and/or are regulated by TP63 (Irf6, Ikkα, Ripk4, Stratifin, and Kdf1) is strikingly similar and involves abnormal balance towards proliferation at the expense of differentiation, but only the first three have corresponding ectodermal phenotypes in humans. We describe a multigenerational Saudi family with an autosomal dominant form of hypohidrotic ectodermal dysplasia in which positional mapping and exome sequencing identified a novel variant in KDF1 that fully segregates with the phenotype. The recapitulation of the phenotype we observe in this family by the Kdf1-/- mouse suggests a causal role played by the KDF1 variant.Entities:
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Year: 2016 PMID: 27838789 DOI: 10.1007/s00439-016-1741-z
Source DB: PubMed Journal: Hum Genet ISSN: 0340-6717 Impact factor: 4.132