Journal article icon

Journal article

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 ...

Expand abstract
Publication status:
Published

Actions


Access Document


Publisher copy:
10.1073/pnas.0909087107

Authors


More by this author
Institution:
University of Oxford
Division:
MSD
Department:
NDM
Sub department:
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:
2010-07-01
DOI:
EISSN:
1091-6490
ISSN:
0027-8424
Source identifiers:
60646
Language:
English
Keywords:
Pubs id:
pubs:60646
UUID:
uuid:f3ac22b4-cb1f-478c-9c6e-d851ee9ebff5
Local pid:
pubs:60646
Deposit date:
2012-12-19

Terms of use


Views and Downloads






If you are the owner of this record, you can report an update to it here: Report update to this record

TO TOP