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A major switch for the Fanconi anemia DNA damage–response pathway

Nature Structural & Molecular Biology volume 15, pages 1128–1130 (2008)Cite this article

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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Figure 1: Activation of the Fanconi anemia pathway.

Katie Ris-Vicari

Figure 2: Models for the switch function of FANCI phosphorylation.

Katie Ris-Vicari

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Acknowledgements

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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  1. 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. wangw@grc.nia.nih.gov,

    Weidong Wang

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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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