期刊
BIOLOGY OPEN
卷 7, 期 3, 页码 -出版社
COMPANY BIOLOGISTS LTD
DOI: 10.1242/bio.031575
关键词
Cell cycle; DNA damage response; Ubiquitin; Protein degradation; CCCH-zinc finger domain; RNA-binding protein
类别
资金
- Japan Society for the Promotion of Science [24112007, 20058001, 15J05603]
- Uehara Memorial Foundation
- Naito Foundation
ZFP36L2 promotes the destruction of AU-rich element-containing transcripts, while its regulation and functional significance in cell cycle control are scarcely identified. We show that ZFP36L2 is a cell cycleregulated CCCH protein, the abundance of which is regulated posttranslationally at the respective stages of the cell cycle. Indeed, ZFP36L2 protein was eliminated after release from M phase, and ZYG11B-based E3 ligase plays a role in its polyubiquitination in interphase. Although ZFP36L2 is dispensable for normal cell cycle progression, we found that endogenous ZFP36L2 played a key role in cisplatin-induced S-phase arrest, a process in which the suppression of G1/S cyclins is necessary. The accumulation of ZFP36L2 was stimulated under DNA replication stresses and altered interactions with a subset of RNA-binding proteins. Notably, silencing endogenous ZFP36L2 led to impaired cell viability in the presence of cisplatin-induced DNA lesions. Thus, we propose that ZFP36L2 is a key protein that controls S-phase progression in the case of genome instability.
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