DNA损伤是电离辐射损伤的核心事件，其修复程度决定细胞放射敏感性。以往的DNA损伤修复研究主要集中于蛋白领域，最新研究显示，长链非编码RNA（lncRNA）在DNA损伤修复启动中发挥不可缺少的作用，为从lncRNA的角度阐释放射损伤的机制提出了新思路。我们筛选发现ANRIL是辐射应答的lncRNA；敲低ANRIL显著抑制了DNA损伤修复，降低了细胞存活率；尤其是同源重组（HR）修复效率降低60%，HR信号通路激活受到显著抑制；并发现ANRIL可以与ATR互作，在ANRIL敲低细胞中照后ATR蛋白发生降解，与泛素化途径有关；ANRIL还可以作为ceRNA参与HR通路的调节。以上研究提示ANRIL介导的HR修复在放射损伤修复中发挥关键作用。本研究将进一步探讨ANRIL在照后HR修复中的作用机制，以及ANRIL对ATR激活和蛋白稳定性的精细调控机制，为放射损伤调控提出新靶点、阐释新机制。

DNA damage is a key mechanism of radiation injury, the repair of which determines radiosensitivity. Many protein factors have been identified in DNA repair previously. However, recently it was proved that long non-coding RNA (lncRNA) exert indispensable roles in DNA damage response, which provide new clues for uncover the mechanism of radiation injury. In present study, our group screened and confirmed a radiation responsive lncRNA, ANRIL. Knockdown of ANRIL reduced cell survival and inhibited DNA repair, of which homologous recombination (HR) repair reduced by 60%. Moreover, we identified that ANRIL bind with ATR and ATR protein degraded in response to ionizing radiation in ANRIL KD cells, which might be related to ubiquitination. Besides, ANRIL also works as ceRNA regulating HR repair. These finding indicates that ANRIL mediated HR repair play key roles in radiation injury repair. In this study, we will investigate the exact mechanism ANRIL in HR repair, as well as the regulatory role on ATR activation and stability. Our work will provide novel mechanisms and target for radiation damage repair.