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Chromatin recruitment of DNA repair proteins: lessons from the fanconi anemia and double-strand break repair pathways.

机译:DNA修复蛋白的染色质募集:来自范可尼贫血和双链断裂修复途径的经验教训。

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摘要

In response to DNA damage, eukaryotic cells must rapidly load DNA repair proteins onto damaged chromatin. Chromatin recruitment often entails ubiquitination of a damage-specific DNA repair protein, interaction with a ubiquitin binding factor, assembly of a multisubunit DNA repair complex, and eventually a deubiquitination event once the DNA repair reaction has been completed. This review focuses on the recent discoveries in the Fanconi Anemia (FA) and DNA double-strand break (DSB) repair pathways, which underscore the importance of regulated chromatin loading in the DNA damage response. Interestingly, these two pathways share several features, suggesting a more general mechanism for DNA-repair regulation.
机译:为了响应DNA损伤,真核细胞必须迅速将DNA修复蛋白上样到受损的染色质上。染色质募集通常需要损伤特异性DNA修复蛋白的泛素化,与泛素结合因子的相互作用,多亚基DNA修复复合物的组装,以及一旦DNA修复反应完成就最终发生去泛素化事件。这篇综述着重于Fanconi贫血(FA)和DNA双链断裂(DSB)修复途径的最新发现,它们强调了在DNA损伤反应中调节染色质负载的重要性。有趣的是,这两种途径共有几个特征,这提示了DNA修复调控的一般机制。

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