中文摘要：

DNA 损坏反应(DDR ) 在之中维持当使动摇时，预先安排的染色体稳定性的机制最重要机关到癌症。可逆 phosphorylation 由蛋白质 kinases 和蛋白质磷酸酶调停了，调整大多数并非所有，细胞的活动，包括 DDR。蛋白质 kinase 禁止者成为了指向的治疗和 anticancer 药开发的主要焦点。然而，我们蛋白质磷酸酶功能的有限知识正在损害我们的能力对磷酸酶开发治疗学的代理人。在这评论，我们总结涉及 DDR 的 serine/threonine 蛋白质磷酸酶的角色并且由蛋白质磷酸酶在邻蛋白质的 situ dephosphorylation 建议那，而不是邻蛋白质的调停 proteasome 的降级，被房间主要采用。

英文摘要：

DNA damage response （DDR） is among the most important of the mechanisms that maintain genome stability which, when destabilized, predisposes organs to cancer. Reversible phosphorylation mediated by protein kinases and protein phosphatases regu- lates most, if not all, cellular activities, including DDR. Protein kinase inhibitors have become the main focus of targeted therapy and anticancer drug development. However, our limited knowledge of protein phosphatase function is compromising our capacity to develop therapeutic agents against phosphatases. In this review, we summarize the roles of serine/threonine protein phosphatases involved in DDR and propose that in situ dephosphorylation of phosphoproteins by protein phosphatases, instead of pro- teasome-mediated degradation of phosphoproteins, is mainly employed by cells.