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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I thank D. Schlessinger for critical reading of the manuscript. The work in the Wang group is supported in part by the Intramural Research Program of the National Institute on Aging, National Institutes of Health, and by the Fanconi Anemia Research Foundation.
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Wang, W. A major switch for the Fanconi anemia DNA damage–response pathway. Nat Struct Mol Biol 15, 1128–1130 (2008). https://doi.org/10.1038/nsmb1108-1128
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