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Binding of double-strand breaks in DNA by human Rad52 protein

Author

Listed:
  • Eric Van Dyck

    (Imperial Cancer Research Fund, Clare Hall Laboratories)

  • Alicja Z. Stasiak

    (Laboratoire d'Analyse Ultrastructurale, Universit de Lausanne)

  • Andrzej Stasiak

    (Laboratoire d'Analyse Ultrastructurale, Universit de Lausanne)

  • Stephen C. West

    (Imperial Cancer Research Fund, Clare Hall Laboratories)

Abstract

Double-strand breaks (DSBs) in DNA are caused by ionizing radiation. These chromosomal breaks can kill the cell unless repaired efficiently, and inefficient or inappropriate repair can lead to mutation, gene translocation and cancer1. Two proteins that participate in the repair of DSBs are Rad52 and Ku: in lower eukaryotes such as yeast, DSBs are repaired by Rad52-dependent homologous recombination, whereas vertebrates repair DSBs primarily by Ku-dependent non-homologous end-joining2. The contribution of homologous recombination to vertebrate DSB repair, however, is important3,4. Biochemical studies indicate that Ku binds to DNA ends and facilitates end-joining5. Here we show that human Rad52, like Ku, binds directly to DSBs, protects them from exonuclease attack and facilitates end-to-end interactions. Amodel for repair is proposed in which either Ku or Rad52 binds the DSB. Ku directs DSBs into the non-homologous end-joining repair pathway, whereas Rad52 initiates repair by homologous recombination. Ku and Rad52, therefore, direct entry into alternative pathways for the repair of DNA breaks.

Suggested Citation

  • Eric Van Dyck & Alicja Z. Stasiak & Andrzej Stasiak & Stephen C. West, 1999. "Binding of double-strand breaks in DNA by human Rad52 protein," Nature, Nature, vol. 398(6729), pages 728-731, April.
    • Handle: RePEc:nat:nature:v:398:y:1999:i:6729:d:10.1038_19560
    DOI: 10.1038/19560
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    Cited by:

    1. Shinta Saito & Noritaka Adachi, 2024. "Characterization and regulation of cell cycle-independent noncanonical gene targeting," Nature Communications, Nature, vol. 15(1), pages 1-13, December.

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