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Dominant mutations in KBTBD13, a member of the BTB/Kelch family, cause nemaline myopathy with cores
Journal article   Peer reviewed

Dominant mutations in KBTBD13, a member of the BTB/Kelch family, cause nemaline myopathy with cores

N. Sambuughin, K.S. Yau, M. Olivé, R.M. Duff, M. Bayarsaikhan, S. Lu, L. Gonzalez-Mera, P. Sivadorai, K.J. Nowak, G. Ravenscroft, …
The American Journal of Human Genetics, Vol.87(6), pp.842-847
2010
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Abstract

We identified a member of the BTB/Kelch protein family that is mutated in nemaline myopathy type 6 (NEM6), an autosomal-dominant neuromuscular disorder characterized by the presence of nemaline rods and core lesions in the skeletal myofibers. Analysis of affected families allowed narrowing of the candidate region on chromosome 15q22.31, and mutation screening led to the identification of a previously uncharacterized gene, KBTBD13, coding for a hypothetical protein and containing missense mutations that perfectly cosegregate with nemaline myopathy in the studied families. KBTBD13 contains a BTB/POZ domain and five Kelch repeats and is expressed primarily in skeletal and cardiac muscle. The identified disease-associated mutations, C.742C>A (p.Arg248Ser), c.1170G>C (p.Lys390Asn), and c.1222C>T (p.Arg408Cys), located in conserved domains of Kelch repeats, are predicted to disrupt the molecule's beta-propeller blades. Previously identified BTB/POZ/Kelch-domain-containing proteins have been implicated in a broad variety of biological processes, including cytoskeleton modulation, regulation of gene transcription, ubiquitination, and myofibril assembly. The functional role of KBTBD13 in skeletal muscle and the pathogenesis of NEM6 are subjects for further studies.

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Collaboration types
Domestic collaboration
International collaboration
Citation topics
1 Clinical & Life Sciences
1.96 Cell Biology
1.96.492 Myosin
Web Of Science research areas
Genetics & Heredity
ESI research areas
Molecular Biology & Genetics
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