ATR/Mec1: coordinating fork stability and repair
ATR/Mec1: coordinating fork stability and repair
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DOI：
10.1016/j.ceb.2009.01.017
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发表时间：
2009-04-01
影响因子：
7.5
通讯作者：
Gasser, Susan M.
中科院分区：
文献类型：
--
作者：
Friedel, Anna M.;Pike, Brietta L.;Gasser, Susan M.
在S期，真核细胞展开并复制大量的DNA，产生对内源性和外源性损伤都非常敏感的结构。DNA聚合酶与受损DNA或其他分叉进展障碍物的碰撞产生复制应激，如果复制体组分不稳定，则可演变成分叉崩溃。为了确保gnome的完整性，停滞的复制叉由一个检查点识别，其中心参与者是S中的人类激酶ATR或Mec 1。啤酒。这篇综述将讨论最近的研究结果揭示的ATIR/Mec 1激酶的作用：无论是在稳定复制体直接和激活检查点响应，以调节起源发射，DNA修复，叉重新启动，和细胞周期的进展。
During S phase, eukaryotic cells unwind and duplicate a tremendous amount of DNA, generating structures that are very sensitive to both endogenous and exogenous insults. The collision of DNA polymerases with damaged DNA or other obstructions to fork progression generates replication stress, which can evolve into fork collapse if the replisome components are not stabilized. To ensure gnome integrity, stalled replication forks are recognized by a checkpoint, whose central player is the human kinase ATR or Mec1 in S. cerevisiae. This review will discuss recent findings revealing roles of the ATIR/Mec1 kinase: both in stabilizing the replisome directly and in activating the checkpoint response to regulate origin firing, DNA repair, fork restart, and cell cycle progression.