News and Views
Nature Structural & Molecular Biology 15, 1128 - 1130 (2008)
doi:10.1038/nsmb1108-1128
A major switch for the Fanconi anemia DNA damage–response pathway
Weidong Wang1
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Weidong Wang is at the Laboratory of Genetics, National Institute on Aging, National Institutes of Health, NIH Biomedical Research Center, Room 10B113, 251 Bayview Boulevard, Baltimore, Maryland 21224, USA.
e-mail: wangw@grc.nia.nih.gov
Abstract
The Fanconi anemia pathway is part of the DNA-damage network including breast cancer–susceptibility proteins BRCA1 and BRCA2. This pathway is activated by the ataxia telangiectasia and Rad3–related (ATR) kinase, but the underlying mechanism remains unclear. A new study demonstrates that a major switch activating the pathway is the ATR-dependent phosphorylation of FANCI.
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