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MMSET regulates histone H4K20 methylation and 53BP1 accumulation at DNA damage sites

Author

Listed:
  • Huadong Pei

    (Mayo Clinic)

  • Lindsey Zhang

    (Washington University)

  • Kuntian Luo

    (Mayo Clinic)

  • Yuxin Qin

    (Mayo Clinic)

  • Marta Chesi

    (Comprehensive Cancer Center, Mayo Clinic Arizona)

  • Frances Fei

    (Washington University)

  • P. Leif Bergsagel

    (Comprehensive Cancer Center, Mayo Clinic Arizona)

  • Liewei Wang

    (Mayo Clinic)

  • Zhongsheng You

    (Washington University)

  • Zhenkun Lou

    (Mayo Clinic)

Abstract

DNA-repair pathways defined Recruitment of p53 binding protein 1 (53BP1) to double-strand DNA breaks is an important step in the cellular response to DNA damage. Here, the histone methyltransferase MMSET is shown to be responsible for localized increases in a histone modification that is involved in recruiting 53BP1. The mechanism of MMSET recruitment to DNA damage sites is also investigated.

Suggested Citation

  • Huadong Pei & Lindsey Zhang & Kuntian Luo & Yuxin Qin & Marta Chesi & Frances Fei & P. Leif Bergsagel & Liewei Wang & Zhongsheng You & Zhenkun Lou, 2011. "MMSET regulates histone H4K20 methylation and 53BP1 accumulation at DNA damage sites," Nature, Nature, vol. 470(7332), pages 124-128, February.
    • Handle: RePEc:nat:nature:v:470:y:2011:i:7332:d:10.1038_nature09658
    DOI: 10.1038/nature09658
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    Cited by:

    1. 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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