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A mechanism for the suppression of homologous recombination in G1 cells

Author

Listed:
  • Alexandre Orthwein

    (The Lunenfeld-Tanenbaum Research Institute, Mount Sinai Hospital, 600 University Avenue)

  • Sylvie M. Noordermeer

    (The Lunenfeld-Tanenbaum Research Institute, Mount Sinai Hospital, 600 University Avenue)

  • Marcus D. Wilson

    (The Lunenfeld-Tanenbaum Research Institute, Mount Sinai Hospital, 600 University Avenue)

  • Sébastien Landry

    (The Lunenfeld-Tanenbaum Research Institute, Mount Sinai Hospital, 600 University Avenue)

  • Radoslav I. Enchev

    (ETH Zurich, Institute of Biochemistry)

  • Alana Sherker

    (The Lunenfeld-Tanenbaum Research Institute, Mount Sinai Hospital, 600 University Avenue
    University of Toronto)

  • Meagan Munro

    (The Lunenfeld-Tanenbaum Research Institute, Mount Sinai Hospital, 600 University Avenue)

  • Jordan Pinder

    (Dalhousie University)

  • Jayme Salsman

    (Dalhousie University)

  • Graham Dellaire

    (Dalhousie University)

  • Bing Xia

    (Rutgers Cancer Institute of New Jersey and Robert Wood Johnson Medical School, Rutgers, The State University of New Jersey)

  • Matthias Peter

    (ETH Zurich, Institute of Biochemistry)

  • Daniel Durocher

    (The Lunenfeld-Tanenbaum Research Institute, Mount Sinai Hospital, 600 University Avenue
    University of Toronto)

Abstract

A mechanism for the repression of homologous recombination in G1, the stage of the cell cycle preceding replication, is determined; the critical aspects are the interaction between BRCA1 and PALB2–BRCA2, and suppression of DNA-end resection.

Suggested Citation

  • Alexandre Orthwein & Sylvie M. Noordermeer & Marcus D. Wilson & Sébastien Landry & Radoslav I. Enchev & Alana Sherker & Meagan Munro & Jordan Pinder & Jayme Salsman & Graham Dellaire & Bing Xia & Matt, 2015. "A mechanism for the suppression of homologous recombination in G1 cells," Nature, Nature, vol. 528(7582), pages 422-426, December.
  • Handle: RePEc:nat:nature:v:528:y:2015:i:7582:d:10.1038_nature16142
    DOI: 10.1038/nature16142
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    Citations

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    Cited by:

    1. Lorenzo Galanti & Martina Peritore & Robert Gnügge & Elda Cannavo & Johannes Heipke & Maria Dilia Palumbieri & Barbara Steigenberger & Lorraine S. Symington & Petr Cejka & Boris Pfander, 2024. "Dbf4-dependent kinase promotes cell cycle controlled resection of DNA double-strand breaks and repair by homologous recombination," Nature Communications, Nature, vol. 15(1), pages 1-19, December.
    2. Jun Dai & Shuyu Zheng & Matías M. Falco & Jie Bao & Johanna Eriksson & Sanna Pikkusaari & Sofia Forstén & Jing Jiang & Wenyu Wang & Luping Gao & Fernando Perez-Villatoro & Olli Dufva & Khalid Saeed & , 2024. "Tracing back primed resistance in cancer via sister cells," Nature Communications, Nature, vol. 15(1), pages 1-14, December.
    3. Bert Kooij & Fenna J. Wal & Magdalena B. Rother & Wouter W. Wiegant & Pau Creixell & Merula Stout & Brian A. Joughin & Julia Vornberger & Matthias Altmeyer & Marcel A. T. M. Vugt & Michael B. Yaffe & , 2024. "The Fanconi anemia core complex promotes CtIP-dependent end resection to drive homologous recombination at DNA double-strand breaks," Nature Communications, Nature, vol. 15(1), pages 1-17, December.
    4. Maria Pilar Sanchez-Bailon & Soo-Youn Choi & Elizabeth R. Dufficy & Karan Sharma & Gavin S. McNee & Emma Gunnell & Kelly Chiang & Debashish Sahay & Sarah Maslen & Grant S. Stewart & J. Mark Skehel & I, 2021. "Arginine methylation and ubiquitylation crosstalk controls DNA end-resection and homologous recombination repair," Nature Communications, Nature, vol. 12(1), pages 1-18, December.

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