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首页> 外文期刊>Journal of Molecular Biology >The two DNA clamps rad9/rad1/hus1 complex and proliferating cell nuclear antigen differentially regulate flap endonuclease 1 activity.
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The two DNA clamps rad9/rad1/hus1 complex and proliferating cell nuclear antigen differentially regulate flap endonuclease 1 activity.

机译：这两个DNA钳rad9 / rad1 / hus1复合体和增殖细胞核抗原差异性调节皮瓣内切核酸酶1活性。

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摘要

DNA damage leads to activation of several mechanisms such as DNA repair and cell-cycle checkpoints. It is evident that these different cellular mechanisms have to be finely co-ordinated. Growing evidence suggests that the Rad9/Rad1/Hus1 cell-cycle checkpoint complex (9-1-1 complex), which is recruited to DNA lesion upon DNA damage, plays a major role in DNA repair. This complex has been shown to interact with and stimulate several proteins involved in long-patch base excision repair. On the other hand, the well-characterised DNA clamp-proliferating cell nuclear antigen (PCNA) also interacts with and stimulates several of these factors. In this work, we compared the effects of the 9-1-1 complex and PCNA on flap endonuclease 1 (Fen1). Our data suggest that PCNA and the 9-1-1 complex can independently bind to and activate Fen1. Finally, acetylation of Fen1 by p300-HAT abolished the stimulatory effect of the 9-1-1 complex but not that of PCNA, suggesting a possible mechanism of regulation of this importantrepair pathway.
机译：DNA损伤导致激活多种机制，例如DNA修复和细胞周期检查点。显然，这些不同的细胞机制必须很好地协调。越来越多的证据表明，在DNA损伤后募集到DNA损伤的Rad9 / Rad1 / Hus1细胞周期检查点复合物（9-1-1复合物）在DNA修复中起主要作用。该复合物已经显示出与长距离碱基切除修复相关的几种蛋白质相互作用并刺激它们。另一方面，特征明确的DNA钳增殖细胞核抗原（PCNA）也与其中的一些因子相互作用并刺激这些因子。在这项工作中，我们比较了9-1-1复合物和PCNA对皮瓣内切核酸酶1（Fen1）的影响。我们的数据表明PCNA和9-1-1复合物可以独立结合并激活Fen1。最后，p300-HAT对Fen1的乙酰化作用消除了9-1-1复合物的刺激作用，但没有消除PCNA的刺激作用，提示了对该重要修复途径进行调控的可能机制。

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