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

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

References

  1. Wang, W. Nat. Rev. Genet. 8, 735–748 (2007).

    Article  CAS  Google Scholar 

  2. Ishiai, M. et al. Nat. Struct. Mol. Biol. 15, 1138–1146 (2008).

    Article  CAS  Google Scholar 

  3. Meetei, A.R. et al. Nat. Genet. 35, 165–170 (2003).

    Article  CAS  Google Scholar 

  4. Gari, K., Decaillet, C., Stasiak, A.Z., Stasiak, A. & Constantinou, A. Mol. Cell 29, 141–148 (2008).

    Article  CAS  Google Scholar 

  5. Gari, K., Decaillet, C., Delannoy, M., Wu, L. & Constantinou, A. Proc. Natl. Acad. Sci. USA published online, doi:10.1073/pnas.0804777105 (8 October 2008).

  6. Sun, W. et al. Mol. Cell 32, 118–128 (2008).

    Article  CAS  Google Scholar 

  7. Xue, Y., Li, Y., Guo, R., Ling, C. & Wang, W. Hum. Mol. Genet. 17, 1641–1652 (2008).

    Article  CAS  Google Scholar 

  8. Garcia-Higuera, I. et al. Mol. Cell 7, 249–262 (2001).

    Article  CAS  Google Scholar 

  9. Ho, G.P., Margossian, S., Taniguchi, T. & D'Andrea, A.D. Mol. Cell. Biol. 26, 7005–7015 (2006).

    Article  CAS  Google Scholar 

  10. Smogorzewska, A. et al. Cell 129, 289–301 (2007).

    Article  CAS  Google Scholar 

  11. Yaffe, M.B. & Smerdon, S.J. Annu. Rev. Biophys. Biomol. Struct. 33, 225–244 (2004).

    Article  CAS  Google Scholar 

  12. Nijman, S.M. et al. Mol. Cell 17, 331–339 (2005).

    Article  CAS  Google Scholar 

  13. Cohn, M.A. et al. Mol. Cell 28, 786–797 (2007).

    Article  CAS  Google Scholar 

  14. Meulmeester, E., Pereg, Y., Shiloh, Y. & Jochemsen, A.G. Cell Cycle 4, 1166–1170 (2005).

    Article  CAS  Google Scholar 

  15. Brenkman, A.B. et al. Cancer Res. 68, 7597–7605 (2008).

    Article  CAS  Google Scholar 

Download references

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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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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