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首页> 外文期刊>Cell cycle >Artemis links ATM to double strand break rejoining.
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Artemis links ATM to double strand break rejoining.

机译：Artemis将ATM连接到双链断裂重新连接。

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摘要

Ataxia telangiectasia mutated protein (ATM) is a damage response kinase that initiates a signal transduction response to the presence of DNA double strand breaks (DSBs) regulating cell cycle checkpoint arrest and apoptosis. Indirect evidence has argued that A-T cells also harbour a repair defect since unrepaired DSBs can be observed in non-replicating A-T cells after ionising radiation (IR). The basis underlying such a repair defect has remained unexplained, however. Artemis, a nuclease, whose activity is modified by phosphorylation in vitro, was recently identified as a novel ATM substrate. Artemis and ATM function in a common pathway required for the processing of a subset of double stranded DNA ends induced by IR prior to rejoining by non-homologous end-joining (NHEJ). This subset of DSBs are those normally rejoined with slow kinetics. Additional components of the ATM signal transduction pathway, Nbs1, Mre11, H2AX and 53BP1, are also required for this component of DSB repair. This process substantially contributes to survival post irradiation. Our findings add a new dimension to the ATM signal transduction response demonstrating ATM-dependent regulation of an end-processing mechanism that functions during the cell cycle delay effected by ATM.
机译：共济失调毛细血管扩张症突变蛋白（ATM）是一种损伤反应激酶，可对调节细胞周期检查点停滞和凋亡的DNA双链断裂（DSB）引发信号传导应答。间接证据表明，A-T细胞也具有修复缺陷，因为电离辐射（IR）后在非复制A-T细胞中可以观察到未修复的DSB。但是，这种修复缺陷的基础仍然无法解释。最近被鉴定为其活性通过体外磷酸化修饰的核酸酶Artemis是新型ATM底物。 Artemis和ATM在通过非同源末端连接（NHEJ）重新连接之前处理IR诱导的双链DNA末端子集所需的通用途径中发挥作用。 DSB的这个子集是通常以缓慢的动力学重新结合的那些。 DSB修复的此组件还需要ATM信号转导途径的其他组件Nbs1，Mre11，H2AX和53BP1。该过程基本上有助于辐射后的存活。我们的发现为ATM信号转导响应增加了新的维度，表明了在ATM引起的细胞周期延迟期间起作用的末端处理机制的ATM依赖性调节。

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