News and Views
Nature Genetics 41, 866 - 868 (2009)
doi:10.1038/ng0809-866
Life can be stressful without ATR
Mark O'Driscoll1
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Mark O'Driscoll is in the Cancer Research UK Human DNA Damage Response Disorders Group, Genome Damage & Stability Centre, University of Sussex, UK.
e-mail: m.o-driscoll@sussex.ac.uk
Abstract
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.
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Manganese Superoxide Dismutase Affects Cytochrome c Release and Caspase-9 Activation After Transient Focal Cerebral Ischemia in MiceJournal of Cerebral Blood Flow & Metabolism Original Article
A mouse model of ATR-Seckel shows embryonic replicative stress and accelerated agingNature Genetics Article (01 Aug 2009)
Regulation of mitotic entry by microcephalin and its overlap with ATR signallingNature Cell Biology Letter (01 Jul 2006)
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