期刊
FEBS LETTERS
卷 591, 期 6, 页码 842-853出版社
WILEY
DOI: 10.1002/1873-3468.12596
关键词
DNA damage; DNA repair; DYRK2; RNF8; gamma H2AX monoubiquitination
资金
- JSPS KAKENHI [JP26290041]
- Jikei University Graduate Research Fund
- Takeda Science Foundation
- Vehicle Racing Commemorative Foundation
- Princess Takamatsu Cancer Research Fund
- Uehara Memorial Foundation
- Nakajima Foundation
- Sagawa Foundation for Promotion of Cancer Research
The genome of eukaryotic cells is frequently exposed to damage by various genotoxins. Phosphorylation of histone H2AX at Serine 139 (gamma- H2AX) is a hallmark of DNA damage. RNF8 monoubiquitinates gamma- H2AX with the Lys63-linked ubiquitin chain to tether DNA repair molecules at DNA lesions. A high-throughput screening identified RNF8 as a binding partner of dual-specificity tyrosine phosphorylation-regulated kinase 2 (DYRK2). Notably, DNA damage-induced monoubiquitination of gamma- H2AX is impaired in DYRK2-depleted cells. The foci formation of p53-binding protein 1 at DNA double-strand break sites is suppressed in DYRK2 knockdown cells, which fail to repair the DNA damage. A homologous recombination assay showed decreased repair efficiency in DYRK2-depleted cells. Our findings indicate direct interaction of DYRK2 with RNF8 in regulating response to DNA damage.
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