中文摘要：

分区有缺陷者 3 (Par3 ) ，在 conservedPar3/Par6/aPKC 建筑群的一个关键部件，在房间极性的戏基础角色。此处，我们报导 Ku70 和通过试管内绑定试金的蛋白质由液体层析双人脚踏车质谱法跟随了的 Ku80 同样新奇的交往 Par3 的鉴定。Ku70/Ku80 蛋白质是 DNA 依赖的蛋白激酶(DNA-PK ) 的二个关键规章的子单元，它在修理双海滨脱氧核糖核酸裂缝(DSB ) 起一个必要作用。我们决定 Par3 withKu70/Ku80 的原子协会被 y 照耀(红外) 提高，有势力 DSB inducer。而且， DNA-PKcs， DNA-PK 的催化子单元，响应红外与 Par3/Ku70/Ku80 建筑群交往了。Par3over 表示或击倒分别地能够 up- 或 downregulat-ing DNA-PK 活动。而且， Par3 击倒的房间被发现在随机的原生质标志集成有缺点，在 DSB 修理追随者红外有缺点、对射线敏感，类似于 Ku70knockdown 房间的显型。这些调查结果作为 DNA-PK 建筑群的一个新奇部件识别 Par3 并且含有到 DSB 修理的房间极性的一个意外连接。

英文摘要：

The partitioning-defective 3 （Par3）, a key component in the conserved Par3/Par6/aPKC complex, plays fundamental roles in cell polarity. Herein we report the identification of Ku70 and Ku80 as novel Par3-interacting proteins through an in vitro binding assay followed by liquid chromatography-tandem mass spectrometry. Ku70/Ku80 proteins are two key regulatory subunits of the DNA-dependent protein kinase （DNA-PK）, which plays an essential role in repairing double-strand DNA breaks （DSBs）. We determined that the nuclear association of Par3 with Ku70/Ku80 was enhanced by γ-irradiation （IR）, a potent DSB inducer. Furthermore, DNA-PKcs, the catalytic subunit of DNA-PK, interacted with the Par3/Ku70/Ku80 complex in response to IR. Par3 over-expression or knockdown was capable of up- or downregulating DNA-PK activity, respectively. Moreover, the Par3 knockdown cells were found to be defective in random plasmid integration, defective in DSB repair following IR, and radiosensitive, phenotypes similar to that of Ku70 knockdown cells. These findings identify Par3 as a novel component of the DNA-PK complex and implicate an unexpected link of cell polarity to DSB repair.