中文摘要：

DNA 双海滨裂缝整个加入的非相应的结束(NHEJ ) 或相应再结合修理(HRR ) 被修理小径。双海滨裂缝修理(DSBR ) 的描绘得好的规章的机制主要在复杂修理蛋白质相互作用和修正的水平被发现。在 transcriptional 水平的 DSBR 的规定也被报导。在这研究，我们发现 DSBR 能被 miR-34a 在 post-transcriptional 水平调整。明确地， miR-34a，能被 DNA 损坏激活，镇压由在有教养的房间损害 NHEJ 和 HRR 小径的 DSBR 活动。压抑主要通过指向支持因素 SIRT1 的批评 DSBR，当没有 3-UTR 的宫外地表示的 SIRT1 能在 DSBR 上救 miR-34a 的禁止的角色。进一步的研究证明 SIRT1 相反地镇压 miR-34a 表示。一起拿，我们 miR-34a 是在 miR-34a 和 SIRT1 之间的 DSBR 和相互的抑制的一个新抑压者的数据表演可以贡献 DNA 损坏修理的规定。

英文摘要：

DNA double-strand breaks are repaired through either non-homologous end joining （NHEJ） or homologous recombination repair （HRR） pathway. The well-characterized regulatory mechanisms of double-strand break repair （DSBR） axe mainly found at the level of complicated repair protein interactions and modifications. Regulation of DSBR at the transcriptional level was also reported. In this study, we found that DSBR can be regulated by miR-34a at the post-transcriptional level. Specifically, miR-34a, which can be activated by DNA damages, represses DSBR activities by impairing both NHEJ and HRR pathways in cultured cells. The repression is mainly through targeting the critical DSBR promoting factor SIRT1, as ectopically expressed SIRT1 without 3＇-UTR can rescue the inhibitory roles of miR-34a on DSBR. Further studies demonstrate that SIRT1 conversely represses miR-34a expression. Taken together, our data show that miR-34a is a new repressor of DSBR and the mutual inhibition between miR-34a and SIRT1 may contribute to regulation of DNA damage repair.