Document Detail


Pathological accumulation of atrophin-1 in dentatorubralpallidoluysian atrophy.
MedLine Citation:
PMID:  21577324     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Dentatorubral-pallidoluysian atrophy (DRPLA) is caused by the expansion of polyglutamine (polyQ) in atrophin-1 (ATN1), also known as DRPLA protein. ATN1 is ubiquitously expressed in the central nervous system (CNS), although selective regions of CNS are degenerated in DRPLA, and this selective neuronal damage gives rise to the specific clinical features of DRPLA. Accumulation of mutant ATN1 that carries an expanded polyQ tract seems to be the primary cause of DRPLA neurodegeneration, but it is still unclear how the accumulation of ATN1 leads to neu-rodegeneration. Recently, cleaved fragments of ATN1 were shown to accumulate in the disease models and the brain tissues of patients with DRPLA. Furthermore, proteolytic processing of ATN1 may regulate the intracellular localization of ATN1 and its fragments. Therefore, proteolytic processing of ATN1 may provide clues to disease pathogenesis and hopefully aid in the determination of molecular targets for effective therapeutic approaches for DRPLA.
Authors:
Yasuyo Suzuki; Ikuru Yazawa
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't; Review     Date:  2011-04-25
Journal Detail:
Title:  International journal of clinical and experimental pathology     Volume:  4     ISSN:  1936-2625     ISO Abbreviation:  Int J Clin Exp Pathol     Publication Date:  2011 Apr 
Date Detail:
Created Date:  2011-05-17     Completed Date:  2011-08-16     Revised Date:  2013-05-29    
Medline Journal Info:
Nlm Unique ID:  101480565     Medline TA:  Int J Clin Exp Pathol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  378-84     Citation Subset:  IM    
Affiliation:
Laboratory of Research Resources, Research Institute for Longevity Sciences, National Center for Geriatrics and Gerontology Aichi, Japan.
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MeSH Terms
Descriptor/Qualifier:
Animals
Central Nervous System / metabolism*,  pathology
Disease Models, Animal
Genetic Predisposition to Disease
Humans
Mutation
Myoclonic Epilepsies, Progressive / genetics,  metabolism*,  pathology,  therapy
Nerve Tissue Proteins / genetics,  metabolism*
Peptides / metabolism
Phenotype
Protein Processing, Post-Translational
Up-Regulation
Chemical
Reg. No./Substance:
0/Nerve Tissue Proteins; 0/Peptides; 0/atrophin-1; 26700-71-0/polyglutamine
Comments/Corrections

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