Understanding the impact of missense mutations on the structure and function of the EDA gene in X‐linked hypohidrotic ectodermal dysplasia: A bioinformatics approach
Author:
Affiliation:
1. Centre for Genetic Disorders, Institute of Science Banaras Hindu University Varanasi Uttar Pradesh India
Publisher
Wiley
Subject
Cell Biology,Molecular Biology,Biochemistry
Link
https://onlinelibrary.wiley.com/doi/pdf/10.1002/jcb.30186
Reference97 articles.
1. Genetic basis of tooth agenesis;Pekka N;J Exp Zoolog Β Mol Dev Evol B,2009
2. X–linked anhidrotic (hypohidrotic) ectodermal dysplasia is caused by mutation in a novel transmembrane protein;Kere J;Nature Genet,1996
3. Only four genes (EDA1, EDAR, EDARADD, and WNT10A) account for 90% of hypohidrotic/anhidrotic ectodermal dysplasia cases;Cluzeau C;Hum Mutat,2011
4. Mutation in WNT10A is associated with an autosomal recessive ectodermal dysplasia: the odonto‐onycho‐dermal dysplasia;Adaimy L;Am J Hum Genet,2007
5. Whole genome sequencing reveals novel non‐synonymous mutation in ectodysplasin A (EDA) associated with non‐syndromic X‐linked dominant congenital tooth agenesis;Sarkar T;PLoS One,2014
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