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53BP1 promotes non-homologous end joining of telomeres by increasing chromatin mobility

Author

Listed:
  • Nadya Dimitrova

    (The Rockefeller University, 1230 York Avenue, New York, New York 10065, USA)

  • Yi-Chun M. Chen

    (Cold Spring Harbor Laboratory, One Bungtown Road, Cold Spring Harbor, New York 11724, USA)

  • David L. Spector

    (Cold Spring Harbor Laboratory, One Bungtown Road, Cold Spring Harbor, New York 11724, USA)

  • Titia de Lange

    (The Rockefeller University, 1230 York Avenue, New York, New York 10065, USA)

Abstract

DNA repair: 53BP1 puts ends in motion When either exogenous or endogenous double-strand breaks occur, the p53 binding protein 53BP1 is one of the earliest proteins to be recruited to the site of the break. 53BP1 helps to promote rejoining of DNA ends during class switch recombination; in a pair of papers in this week's Nature, the laboratories of André Nussenzweig and Titia de Lange show it is also required for V(D)J recombination and for joining of DNA breaks in telomeres. In V(D)J recombination, the ends of the programmed double-strand break are degraded when 53BP1 is absent, and joining between distal V and DJ segments is affected. At broken telomeres, 53BP1 increases the volume of the nucleus searched by the DNA ends so that they are more likely to encounter a partner to which they can be ligated. Thus, 53BP1 facilitates repair by changing the dynamics of movement of broken ends, making long-range interactions more frequent.

Suggested Citation

  • Nadya Dimitrova & Yi-Chun M. Chen & David L. Spector & Titia de Lange, 2008. "53BP1 promotes non-homologous end joining of telomeres by increasing chromatin mobility," Nature, Nature, vol. 456(7221), pages 524-528, November.
    • Handle: RePEc:nat:nature:v:456:y:2008:i:7221:d:10.1038_nature07433
    DOI: 10.1038/nature07433
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    Cited by:

    1. Uta Eberlein & Michel Peper & Maria Fernández & Michael Lassmann & Harry Scherthan, 2015. "Calibration of the γ-H2AX DNA Double Strand Break Focus Assay for Internal Radiation Exposure of Blood Lymphocytes," PLOS ONE, Public Library of Science, vol. 10(4), pages 1-11, April.
    2. Jin H. Yang & Hugo B. Brandão & Anders S. Hansen, 2023. "DNA double-strand break end synapsis by DNA loop extrusion," Nature Communications, Nature, vol. 14(1), pages 1-14, December.
    3. Jian Ma & Yingke Zhou & Penglin Pan & Haixin Yu & Zixi Wang & Lei Lily Li & Bing Wang & Yuqian Yan & Yunqian Pan & Qi Ye & Tianjie Liu & Xiaoyu Feng & Shan Xu & Ke Wang & Xinyang Wang & Yanlin Jian & , 2023. "TRABID overexpression enables synthetic lethality to PARP inhibitor via prolonging 53BP1 retention at double-strand breaks," Nature Communications, Nature, vol. 14(1), pages 1-12, December.

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