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Autoimmune Disease in a DFNA6/14/38 Family carrying a Novel Missense Mutation in WFS1
Journal article   Peer reviewed

Autoimmune Disease in a DFNA6/14/38 Family carrying a Novel Missense Mutation in WFS1

Michael S Hildebrand, Jessica L Sorensen, Maren Jensen, William J Kimberling and Richard J.H Smith
American journal of medical genetics. Part A, Vol.146A(17), pp.2258-2265
09/01/2008
DOI: 10.1002/ajmg.a.32449
PMCID: PMC2586182
PMID: 18688868

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Abstract

Most familial cases of autosomal dominant low frequency sensorineural hearing loss (LFSNHL) are attributable to mutations in the Wolframin syndrome 1 ( WFS1 ) gene at the DFNA6/14/38 locus. WFS1 mutations at this locus were first described in 2001 in six families segregating LFSNHL that was non-progressive below 2000 Hz; the causative mutations all clustered in the C-terminal domain of the wolframin protein. Mutations in WFS1 also cause Wolfram syndrome (WS), an autosomal recessive neurodegenerative disorder defined by diabetes mellitus, optic atrophy and often deafness, while numerous single nucleotide polymorphisms (SNPs) in WFS1 have been associated with increased risk for diabetes mellitus, psychiatric illnesses and Parkinson’s disease. This study was conducted in an American family segregating autosomal dominant LFSNHL. Two hearing impaired family members also had autoimmune diseases - Graves disease (GD) and Crohn’s disease (CD). Based on the low frequency audioprofile, mutation screening of WFS1 was completed and a novel missense mutation (c.2576G→A) that results in an arginine-to-glutamine substitution (p.R859Q) was identified in the C-terminal domain of the wolframin protein where most LFSNHL-causing mutations cluster. The family member with GD also carried polymorphisms in WFS1 that have been associated with other autoimmune diseases.
14 Missense mutation 38 WFS1 Graves disease DFNA6 Crohn’s disease

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