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CtIP-BRCA1 modulates the choice of DNA double-strand-break repair pathway throughout the cell cycle

Author

Listed:
  • Maximina H. Yun

    (MRC Laboratory of Molecular Biology, Hills Road, Cambridge CB2 0QH, UK)

  • Kevin Hiom

    (MRC Laboratory of Molecular Biology, Hills Road, Cambridge CB2 0QH, UK)

Abstract

DNA repair: the chosen pathway Cells have two main DNA repair pathways, homologous recombination and end-joining, that were thought to function in different stages of the cell cycle. How the cell recognizes these stages and switches its predominant repair pathway is not well known. In this work, Maximina Yun and Kevin Hiom show that CtIP, a protein recently identified as a participant in the resection of broken DNA ends, serves to switch between these pathways. They show that as cells enter the cell stage that replicates DNA, CtIP undergoes a specific phosphorylation that recruits the breast cancer susceptibility protein, BRCA1, and this directs the cell to use homologous recombination.

Suggested Citation

  • Maximina H. Yun & Kevin Hiom, 2009. "CtIP-BRCA1 modulates the choice of DNA double-strand-break repair pathway throughout the cell cycle," Nature, Nature, vol. 459(7245), pages 460-463, May.
  • Handle: RePEc:nat:nature:v:459:y:2009:i:7245:d:10.1038_nature07955
    DOI: 10.1038/nature07955
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    Cited by:

    1. Martin Peterka & Nina Akrap & Songyuan Li & Sandra Wimberger & Pei-Pei Hsieh & Dmitrii Degtev & Burcu Bestas & Jack Barr & Stijn Plassche & Patricia Mendoza-Garcia & Saša Šviković & Grzegorz Sienski &, 2022. "Harnessing DSB repair to promote efficient homology-dependent and -independent prime editing," Nature Communications, Nature, vol. 13(1), pages 1-9, December.
    2. Daipayan Banerjee & Kurt Langberg & Salar Abbas & Eric Odermatt & Praveen Yerramothu & Martin Volaric & Matthew A. Reidenbach & Kathy J. Krentz & C. Dustin Rubinstein & David L. Brautigan & Tarek Abba, 2021. "A non-canonical, interferon-independent signaling activity of cGAMP triggers DNA damage response signaling," Nature Communications, Nature, vol. 12(1), pages 1-24, December.

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