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Isolated short CTG/CAG DNA slip-outs are repaired efficiently by hMutSbeta, but clustered slip-outs are poorly repaired.

Abstract:

Expansions of CTG/CAG trinucleotide repeats, thought to involve slipped DNAs at the repeats, cause numerous diseases including myotonic dystrophy and Huntington's disease. By unknown mechanisms, further repeat expansions in transgenic mice carrying expanded CTG/CAG tracts require the mismatch repair (MMR) proteins MSH2 and MSH3, forming the MutSbeta complex. Using an in vitro repair assay, we investigated the effect of slip-out size, with lengths of 1, 3, or 20 excess CTG repeats, as well as ...

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Publication status:
Published

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Publisher copy:
10.1073/pnas.0909087107

Authors


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Institution:
University of Oxford
Department:
Oxford, MSD, Clinical Medicine, Structural Genomics Consortium
Role:
Author
Journal:
Proceedings of the National Academy of Sciences of the United States of America
Volume:
107
Issue:
28
Pages:
12593-12598
Publication date:
2010-07-05
DOI:
EISSN:
1091-6490
ISSN:
0027-8424
URN:
uuid:f3ac22b4-cb1f-478c-9c6e-d851ee9ebff5
Source identifiers:
60646
Local pid:
pubs:60646

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