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

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.

מידע ביבליוגרפי

Principais autores:	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
פורמט:	Artigo
שפה:	Inglês
יצא לאור:	Nature Portfolio 2023-03-01
סדרה:	Nature Communications
גישה מקוונת:	https://doi.org/10.1038/s41467-023-37499-5
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