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ATM orchestrates the DNA-damage response to counter toxic non-homologous end-joining at broken replication forks.ATM 协调 DNA 损伤反应以对抗断裂复制叉处的有毒非同源末端连接。
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UBQLN4 Represses Homologous Recombination and Is Overexpressed in Aggressive Tumors.UBQLN4 抑制同源重组，在侵袭性肿瘤中过表达。
Cell. 2019 Jan 24;176(3):505-519.e22. doi: 10.1016/j.cell.2018.11.024. Epub 2019 Jan 3.
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Involvement of ATM in homologous recombination after end resection and RAD51 nucleofilament formation.ATM在末端切除和RAD51核丝形成后的同源重组中的作用。
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BLM-DNA2-RPA-MRN and EXO1-BLM-RPA-MRN constitute two DNA end resection machineries for human DNA break repair.BLM-DNA2-RPA-MRN 和 EXO1-BLM-RPA-MRN 构成了人类 DNA 断裂修复的两种 DNA 末端切除机制。
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泛素样蛋白4通过抑制DNA末端切除来促进非同源末端连接。

UBQLN4 promotes non-homologous end joining by repressing DNA end-resection.

作者信息

Jachimowicz Ron D, Reinhardt H Christian

机构信息

Clinic I of Internal Medicine, Faculty of Medicine and University Hospital Cologne, Cologne, Germany.

Cologne Excellence Cluster on Cellular Stress Response in Aging-Associated Diseases, University of Cologne, Cologne, Germany.

出版信息

Mol Cell Oncol. 2019 Feb 20;6(2):1575692. doi: 10.1080/23723556.2019.1575692. eCollection 2019.

DOI:10.1080/23723556.2019.1575692
PMID:31131301
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6512934/
Abstract

Ataxia-telangiectasia-mutated (ATM) promotes homologous recombination (HR)-mediated DNA double-strand break repair. It was recently shown that the proteasomal shuttle factor UBQLN4 facilitates MRE11 degradation to repress HR. Surprisingly, the UBQLN4-MRE11 interaction is ATM-dependent, suggesting that the proximal DNA damage kinase ATM does not only initiate HR, but also limits excessive end resection.

摘要

共济失调毛细血管扩张症突变基因（ATM）促进同源重组（HR）介导的DNA双链断裂修复。最近研究表明，蛋白酶体穿梭因子UBQLN4促进MRE11降解以抑制HR。令人惊讶的是，UBQLN4与MRE11的相互作用依赖于ATM，这表明近端DNA损伤激酶ATM不仅启动HR，还限制过度的末端切除。