Nature Communications (Mar 2023)

TRABID overexpression enables synthetic lethality to PARP inhibitor via prolonging 53BP1 retention at double-strand breaks

  • 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,
  • Bohan Ma,
  • Yizeng Fan,
  • Yang Gao,
  • Haojie Huang,
  • Lei Li

DOI
https://doi.org/10.1038/s41467-023-37499-5
Journal volume & issue
Vol. 14, no. 1
pp. 1 – 12

Abstract

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The retention of 53BP1 at DNA double strand breaks (DSBs) is inhibitory to homologous recombination repair. Following ionising radiation, the authors demonstrate that TRABID-mediated deubiquitination of 53BP1 promotes its retention, sensitising prostate cancer to PARP inhibition.