期刊
TRENDS IN GENETICS
卷 36, 期 12, 页码 981-997出版社
CELL PRESS
DOI: 10.1016/j.tig.2020.01.001
关键词
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资金
- Israel Science Foundation [2255/19]
- Israel Cancer Research fund [7189744]
- ISF-NSFC fund [2511/18]
- Neubauer Family foundation
Defective double-strand break (DSB) repair leads to genomic instabilities that may augment carcinogenesis. DSBs trigger transient transcriptional silencing in the vicinity of transcriptionally active genes through multilayered processes instigated by Ataxia telangiectasia mutated (ATM), DNA-dependent protein kinase (DNA-PK), and poly-(ADP-ribose) polymerase 1 (PARP1). Novel factors have been identified that ensure DSB-induced silencing via two distinct pathways: direct inhibition of RNA Polymerase II (Pol II) mediated by negative elongation factor (NELF), and histone code editing by CDYL1 and histone deacetylases (HDACs) that catalyze H3K27me3 and erase lysine crotonylation, respectively. Here, we highlight major advances in understanding the mechanisms underlying transcriptional silencing at DSBs, and discuss its functional implications on repair. Furthermore, we discuss consequential links between DSBsilencing factors and carcinogenesis and discuss the potential of exploiting them for targeted cancer therapy.
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