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SCA17 homozygote showing Huntington's disease-like phenotype

Published:2004 Issue:2 Volume:55 Page:281-286
ISSN:0364-5134
Container-title:Annals of Neurology
language:en
Short-container-title:Ann Neurol.

Author:

Toyoshima Yasuko,Yamada Mitsunori,Onodera Osamu,Shimohata Mitsuteru,Inenaga Chikanori,Fujita Nobuya,Morita Masahiro,Tsuji Shoji,Takahashi Hitoshi

Publisher

Wiley

Subject

Neurology (clinical),Neurology

Reference18 articles.

1. A neurological disease caused by an expanded CAG trinucleotide repeat in the TATA-binding protein gene: a new polyglutamine disease? [In Process Citation]

2. SCA17, a novel autosomal dominant cerebellar ataxia caused by an expanded polyglutamine in TATA-binding protein

3. CAG repeat expansion in the TATA box-binding protein gene causes autosomal dominant cerebellar ataxia

4. Different types of repeat expansion in the TATA-binding protein gene are associated with a new form of inherited ataxia

5. Trinucleotide Repeats in 202 Families With Ataxia

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1. The New Face of Dynamic Mutation—The CAA [CAG]n CAA CAG Motif as a Mutable Unit in the TBP Gene Causative for Spino-Cerebellar Ataxia Type 17;International Journal of Molecular Sciences;2024-07-26

2. Polyglutamine (PolyQ) Diseases: Navigating the Landscape of Neurodegeneration;ACS Chemical Neuroscience;2024-07-12

3. Hereditary Ataxias: From Bench to Clinic, Where Do We Stand?;Cells;2024-02-09

4. Ataxia;Movement Disorders Phenomenology;2024

5. Complex Ataxia‐Dementia Phenotype in Patients with Digenic TBP/STUB1 Spinocerebellar Ataxia;Movement Disorders;2023-02-17

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