PUM1介导的mRNA降解的抑制在DNA损伤后激活跨损伤合成。
Repression of PUM1-mediated mRNA decay activates translesion synthesis after DNA damage.
作者信息
Yamada Toshimichi, Sun Xiaoning, Akimitsu Nobuyoshi
机构信息
Department of Molecular and Cellular Biochemistry, Meiji Pharmaceutical University, Tokyo, Japan.
Graduate School of Engineering, The University of Tokyo, Tokyo, Japan.
出版信息
Mol Cell Oncol. 2020 Oct 12;7(6):1812868. doi: 10.1080/23723556.2020.1812868. eCollection 2020.
Abstract
Biological roles of Pumilio1 (PUM1) in ubiquitous cells remain unclear. Here we identify 48 degrading target mRNAs by combined analysis of transcriptome-wide mRNA stabilities and the binding of mRNAs. Further analysis revealed that cells respond to DNA damage by inhibiting PUM1-mediated mRNA decay to activate translesion synthesis (46/50).
摘要
Pumilio1（PUM1）在普遍存在的细胞中的生物学作用仍不清楚。在这里，我们通过对全转录组mRNA稳定性和mRNA结合的联合分析，鉴定出48个降解靶标mRNA。进一步分析表明，细胞通过抑制PUM1介导的mRNA衰变来应对DNA损伤，从而激活跨损伤合成（46/50）。
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Systematic Analysis of Targets of Pumilio-Mediated mRNA Decay Reveals that PUM1 Repression by DNA Damage Activates Translesion Synthesis.基于 pumilio 介导的 mRNA 降解靶点的系统分析揭示，DNA 损伤对 pum1 的抑制作用激活了跨损伤合成。
Cell Rep. 2020 May 5;31(5):107542. doi: 10.1016/j.celrep.2020.107542.
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