IDEAS home Printed from https://ideas.repec.org/a/nat/nature/v469y2011i7329d10.1038_nature09585.html
   My bibliography  Save this article

H2AX prevents CtIP-mediated DNA end resection and aberrant repair in G1-phase lymphocytes

Author

Listed:
  • Beth A. Helmink

    (Washington University School of Medicine)

  • Anthony T. Tubbs

    (Washington University School of Medicine)

  • Yair Dorsett

    (Washington University School of Medicine)

  • Jeffrey J. Bednarski

    (Washington University School of Medicine
    Washington University School of Medicine)

  • Laura M. Walker

    (Washington University School of Medicine)

  • Zhihui Feng

    (Washington University School of Medicine)

  • Girdhar G. Sharma

    (Washington University School of Medicine)

  • Peter J. McKinnon

    (St Jude Children’s Research Hospital)

  • Junran Zhang

    (Washington University School of Medicine)

  • Craig H. Bassing

    (Center for Childhood Cancer Research, Children’s Hospital of Philadelphia, University of Pennsylvania School of Medicine, Abramson Family Cancer Research Institute)

  • Barry P. Sleckman

    (Washington University School of Medicine)

Abstract

Role for histone H2AX in maintaining genomic stability Antigen receptor loci contain numerous gene segments that are recombined in response to antigen stimulation. The RAG1/2 complex makes the double-strand breaks that initiate recombination. The ends of these breaks are hairpins that can only be cleaved by the Artemis nuclease. Barry Sleckman and colleagues show that the specificity for Artemis is dictated by the histone variant H2AX, in cooperation with the repair protein MDC1. In the absence of H2AX, another nuclease, CtIP, can open the ends but they are not joined efficiently by classical non-homogeneous end-joining, and this leads to genomic instability.

Suggested Citation

  • Beth A. Helmink & Anthony T. Tubbs & Yair Dorsett & Jeffrey J. Bednarski & Laura M. Walker & Zhihui Feng & Girdhar G. Sharma & Peter J. McKinnon & Junran Zhang & Craig H. Bassing & Barry P. Sleckman, 2011. "H2AX prevents CtIP-mediated DNA end resection and aberrant repair in G1-phase lymphocytes," Nature, Nature, vol. 469(7329), pages 245-249, January.
    • Handle: RePEc:nat:nature:v:469:y:2011:i:7329:d:10.1038_nature09585
    DOI: 10.1038/nature09585
    as

    Download full text from publisher

    File URL: https://www.nature.com/articles/nature09585
    File Function: Abstract
    Download Restriction: Access to the full text of the articles in this series is restricted.
    File URL: https://libkey.io/10.1038/nature09585?utm_source=ideas
    LibKey link: if access is restricted and if your library uses this service, LibKey will redirect you to where you can use your library subscription to access this item
    ---><---

    As the access to this document is restricted, you may want to search for a different version of it.

    Citations

    Citations are extracted by the CitEc Project, subscribe to its RSS feed for this item.
    as


    Cited by:

    1. Diego Dibitetto & Martin Liptay & Francesca Vivalda & Hülya Dogan & Ewa Gogola & Martín González Fernández & Alexandra Duarte & Jonas A. Schmid & Morgane Decollogny & Paola Francica & Sara Przetocka &, 2024. "H2AX promotes replication fork degradation and chemosensitivity in BRCA-deficient tumours," Nature Communications, Nature, vol. 15(1), pages 1-14, December.

    More about this item

    Statistics

    Access and download statistics

    Corrections

    All material on this site has been provided by the respective publishers and authors. You can help correct errors and omissions. When requesting a correction, please mention this item's handle: RePEc:nat:nature:v:469:y:2011:i:7329:d:10.1038_nature09585. See general information about how to correct material in RePEc.

    If you have authored this item and are not yet registered with RePEc, we encourage you to do it here. This allows to link your profile to this item. It also allows you to accept potential citations to this item that we are uncertain about.

    We have no bibliographic references for this item. You can help adding them by using this form .

    If you know of missing items citing this one, you can help us creating those links by adding the relevant references in the same way as above, for each refering item. If you are a registered author of this item, you may also want to check the "citations" tab in your RePEc Author Service profile, as there may be some citations waiting for confirmation.

    For technical questions regarding this item, or to correct its authors, title, abstract, bibliographic or download information, contact: Sonal Shukla or Springer Nature Abstracting and Indexing (email available below). General contact details of provider: http://www.nature.com .

    Please note that corrections may take a couple of weeks to filter through the various RePEc services.

    IDEAS is a RePEc service. RePEc uses bibliographic data supplied by the respective publishers.