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Life can be stressful without ATR.
A new study reports the first mouse model for ATR-mutated Seckel syndrome. The mice show phenotypes recapitulating the human disorder and provide insights into how reduced ATR function affects normal embryonic development by increasing replicative stress, ultimately resulting in an accelerated aging phenotype postnatally. © 2009 Nature America, Inc. All rights reserved.
History
Publication status
- Published
Journal
Nature GeneticsISSN
10614036Publisher
Nature Publishing GroupExternal DOI
Issue
8Volume
41Page range
866-888Department affiliated with
- Sussex Centre for Genome Damage Stability Publications
Full text available
- No
Peer reviewed?
- Yes
Legacy Posted Date
2012-02-06Usage metrics
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