[1]杜利清,刘强,王彦,等.Ku70对同源重组修复蛋白Rad51的调节作用[J].国际放射医学核医学杂志,2013,37(5):272-274.[doi:10.3760/cma.j.issn.1673-4114.2013.05.005]
 DU Li-qing,LIU Qiang,WANG Yan,et al.Regulation of homologous recombination repair protein Rad51 by Ku70[J].International Journal of Radiation Medicine and Nuclear Medicine,2013,37(5):272-274.[doi:10.3760/cma.j.issn.1673-4114.2013.05.005]
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Ku70对同源重组修复蛋白Rad51的调节作用(/HTML)
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《国际放射医学核医学杂志》[ISSN:1673-4114/CN:12-1381/R]

卷:
37
期数:
2013年第5期
页码:
272-274
栏目:
论著
出版日期:
2013-09-25

文章信息/Info

Title:
Regulation of homologous recombination repair protein Rad51 by Ku70
作者:
杜利清 刘强 王彦 徐畅 曹嘉 付岳 陈凤华 樊飞跃
300192 天津, 中国医学科学院放射医学研究所, 天津市分子核医学重点实验室
Author(s):
DU Li-qing LIU Qiang WANG Yan XU Chang CAO Jia FU Yue CHEN Feng-hua FAN Fei-yue
Tianjin Key Laboratory of Molecular Nuclear Medicine, Institute of Radiation Medicine, Chinese Academy of Medical Sciences, Tianjin 300192, China
关键词:
DNA修复Rad51重组酶RNA小分子干扰Ku70
Keywords:
DNA repairRad51 recombinaseRNA small interferingKu70
DOI:
10.3760/cma.j.issn.1673-4114.2013.05.005
摘要:
目的 研究非同源末端连接(NHEJ)蛋白Ku70对同源重组(HR)修复蛋白Rad51的调节作用,初步探讨HR与NHEJ间协同作用的机制。方法 采用Western blot法观察特异性增高和降低Ku70蛋白水平后Rad51蛋白表达水平的变化情况。结果 靶向Ku70基因小干扰RNA(siRNA)单纯转染组Rad51蛋白的表达水平较空白对照组明显下降;Ku70高表达载体PGCsi3.0-hKu70转染肿瘤细胞后,随着Ku70表达水平的升高,Rad51水平也随之升高。结论 Ku70可能对Rad51有正调控作用,NHEJ可能通过Ku70对Rad51的调节来实现其与HR的协同作用。
Abstract:
Objective To explore the regulative effect of non-homologous end joining (NHEJ)protein Ku70 on homologous recombination repair protein Rad51, and to investigate the synergistic mechanism of homologous recombination repair in combination with NHEJ.Methods Observed Rad51 protein expression after transfect Ku70 small interfering RNA or Ku70 plasmid DNA into tumor cells using Western blot.Results Expression of Rad51 was obviously reduced after pretreated with Ku70 small interfering RNA.And with the increasing expression of Ku70 protein after transfection of Ku70 plasmid DNA PGCsi3.0-hKu70 into tumor cell lines, the Rad51 protein expression was increased.Conclusion Ku70 protein has regulating effect on gene expression of Rad51, and it might participate in the collaboration between homologous recombination repair and NHEJ.

参考文献/References:

[1] Mao Z, Bozzella M,Seluanov A, et al. DNA repair by nonhomologous end joining and homologous recombination during cell cycle in human cells. Cell Cycle, 2008, 7(18):2902-2906.
[2] Kass EM, Jasin M. Collaboration and competition between DNA double-strand break repair pathways. FEBS Lett, 2012, 584(17):3703-3708.
[3] Orii KE, Lee Y, Kondo N,et al. Selective utilization of nonhomoio-gous end-joining and homologous recombination DNA repair path-ways during nervous system development. Proc Nall Acad Sci USA,2006,103(26):10017-10022.
[4] Couëdel C, Mills KD, Barchi M, et al. Collaboration of homologous recombination and nonhomologous end-joining factors for the sur-vival and integrity of mice and cells. Genes Dev, 2004, 18(11):1293-1304.
[5] Mills KD, Ferguson DO, Essers J, et al. Rad54 and DNA Ligase IV cooperate to maintain mammalian chromatid stability. Genes Dev,2004,18(11):1283-1292.
[6] Deckbar D, Jeggo PA, Löbrich M. Understanding the limitations of radiation-induced cell cycle checkpoints. Crit Rev Biochem Mol Biol, 2011,46(4):271-283.
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备注/Memo

备注/Memo:
收稿日期:2012-11-07。
基金项目:教育部高等学校博士学科点专项基金(20121106-120043);中国医学科学院放射医学研究所学科发展基金(SF1208),专项基金(1335)
通讯作者:樊飞跃,Email:fan_feiyue@yeah.net
更新日期/Last Update: 1900-01-01