Literature DB >> 11030759

Dramatic mutation instability in HD mouse striatum: does polyglutamine load contribute to cell-specific vulnerability in Huntington's disease?

L Kennedy1, P F Shelbourne.   

Abstract

An unstable CAG triplet repeat expansion encoding a polyglutamine stretch within the ubiquitously expressed protein huntingtin is responsible for causing Huntington's disease (HD). By quantifying the repeat sizes of individual mutant alleles in tissues derived from an accurate genetic mouse model of HD we show that the mutation becomes very unstable in striatal tissue. The expansion-biased changes increase with age, such that some striatal cells from old HD mice contain mutations that have tripled in size. If this pattern of repeat instability is recapitulated in human striatal tissue, the concomitant increased polyglutamine load may contribute to the patterns of selective neuronal cell death in HD. Our findings also suggest that trinucleotide repeat instability can occur by mechanisms that are not replication-based.

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Year:  2000        PMID: 11030759     DOI: 10.1093/hmg/9.17.2539

Source DB:  PubMed          Journal:  Hum Mol Genet        ISSN: 0964-6906            Impact factor:   6.150


  68 in total

Review 1.  Huntington's disease.

Authors:  S Davies; D B Ramsden
Journal:  Mol Pathol       Date:  2001-12

2.  Chemically induced increases and decreases in the rate of expansion of a CAG*CTG triplet repeat.

Authors:  Mário Gomes-Pereira; Darren G Monckton
Journal:  Nucleic Acids Res       Date:  2004-05-20       Impact factor: 16.971

Review 3.  Differential vulnerability of neurons in Huntington's disease: the role of cell type-specific features.

Authors:  Ina Han; YiMei You; Jeffrey H Kordower; Scott T Brady; Gerardo A Morfini
Journal:  J Neurochem       Date:  2010-03-17       Impact factor: 5.372

Review 4.  Current understanding on the pathogenesis of polyglutamine diseases.

Authors:  Xiao-Hui He; Fang Lin; Zheng-Hong Qin
Journal:  Neurosci Bull       Date:  2010-06       Impact factor: 5.203

Review 5.  DNA base excision repair: a mechanism of trinucleotide repeat expansion.

Authors:  Yuan Liu; Samuel H Wilson
Journal:  Trends Biochem Sci       Date:  2012-01-27       Impact factor: 13.807

6.  Modeling Huntington's disease in cells, flies, and mice.

Authors:  S Sipione; E Cattaneo
Journal:  Mol Neurobiol       Date:  2001-02       Impact factor: 5.590

Review 7.  Molecular pathogenesis of spinocerebellar ataxia type 6.

Authors:  Holly B Kordasiewicz; Christopher M Gomez
Journal:  Neurotherapeutics       Date:  2007-04       Impact factor: 7.620

8.  Huntingtin aggregate-associated axonal degeneration is an early pathological event in Huntington's disease mice.

Authors:  H Li; S H Li; Z X Yu; P Shelbourne; X J Li
Journal:  J Neurosci       Date:  2001-11-01       Impact factor: 6.167

9.  Modelling and inference reveal nonlinear length-dependent suppression of somatic instability for small disease associated alleles in myotonic dystrophy type 1 and Huntington disease.

Authors:  Catherine F Higham; Darren G Monckton
Journal:  J R Soc Interface       Date:  2013-09-18       Impact factor: 4.118

10.  Early motor dysfunction and striosomal distribution of huntingtin microaggregates in Huntington's disease knock-in mice.

Authors:  Liliana B Menalled; Jessica D Sison; Ying Wu; Melisa Olivieri; Xiao-Jiang Li; He Li; Scott Zeitlin; Marie-Françoise Chesselet
Journal:  J Neurosci       Date:  2002-09-15       Impact factor: 6.167

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