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A mutation in the α tropomyosin gene TPM3 associated with autosomal dominant nemaline myopathy
Journal article   Peer reviewed

A mutation in the α tropomyosin gene TPM3 associated with autosomal dominant nemaline myopathy

N.G. Laing, S.D. Wilton, P.A. Akkari, S. Dorosz, K. Boundy, C. Kneebone, P. Blumbergs, S. White, H. Watkins, D.R. Love, …
Nature Genetics, Vol.9(1), pp.75-79
1995
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Abstract

Nemaline myopathies are diseases characterized by the presence in muscle fibres of pathognomonic rod bodies. These are composed largely of alpha−actinin and actin. We have identified a missense mutation in the alpha−tropomyosin gene, TPM3, which segregates completely with the disease in a family whose autosomal dominant nemaline myopathy we had previously localized to chromosome 1p13−q25. The mutation substitutes an arginine residue for a highly conserved methionine in a putative actin−binding site near the N terminus of the alpha−tropomyosin. The mutation may strengthen tropomyosin − actin binding, leading to rod body formation, by adding a further basic residue to the postulated actin−binding motif.

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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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