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细胞对 DNA 双链断裂反应中信号转导的结构机制。

Structural mechanisms underlying signaling in the cellular response to DNA double strand breaks.

机构信息

Department of Biochemistry, University of Alberta, Edmonton, AB T6G 2H7, Canada.

出版信息

Mutat Res. 2013 Oct;750(1-2):15-22. doi: 10.1016/j.mrfmmm.2013.07.004. Epub 2013 Jul 27.

DOI:10.1016/j.mrfmmm.2013.07.004
PMID:23896398
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3818410/
Abstract

DNA double strand breaks (DSBs) constitute one of the most dangerous forms of DNA damage. In actively replicating cells, these breaks are first recognized by specialized proteins that initiate a signal transduction cascade that modulates the cell cycle and results in the repair of the breaks by homologous recombination (HR). Protein signaling in response to double strand breaks involves phosphorylation and ubiquitination of chromatin and a variety of associated proteins. Here we review the emerging structural principles that underlie how post-translational protein modifications control protein signaling that emanates from these DNA lesions.

摘要

DNA 双链断裂 (DSBs) 是最危险的 DNA 损伤形式之一。在活跃复制的细胞中，这些断裂首先被专门的蛋白质识别，这些蛋白质启动信号转导级联反应，调节细胞周期，并通过同源重组 (HR) 修复断裂。对双链断裂的蛋白质信号转导涉及染色质和各种相关蛋白质的磷酸化和泛素化。在这里，我们回顾了新兴的结构原则，这些原则是如何控制从这些 DNA 损伤中产生的蛋白质信号转导的。

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