Current topics in DNA double-strand break repair

被引：85

作者：

Kobayashi, Junya ^{[2
]}

Iwabuchi, Kuniyoshi ^{[3
]}

Miyagawa, Kiyoshi ^{[4
]}

Sonoda, Eiichiro ^{[5
]}

Suzuki, Keiji ^{[6
]}

Takata, Minoru ^{[7
]}

Tauchi, Hiroshi ^{[1
]}

机构：

[1] Ibaraki Univ, Fac Sci, Dept Environm Sci, Ibaraki 3108512, Japan

[2] Kyoto Univ, Dept Genome Repair Dynam, Ctr Radiat Biol, Sakyo Ku, Kyoto 6068501, Japan

[3] Kanazawa Med Univ, Dept Biochem, Uchinada, Ishikawa 9200293, Japan

[4] Univ Tokyo, Grad Sch Med, Sect Radiat Biol, Bunkyo Ku, Tokyo 1130033, Japan

[5] Kyoto Univ, Dept Radiat Genet, Fac Med, Sakyo Ku, Kyoto 6068501, Japan

[6] Nagasaki Univ, Grad Sch Biomed Sci, Nagasaki 8528523, Japan

[7] Kyoto Univ, Dept Late Effects Studies, Ctr Radiat Biol, Sakyo Ku, Kyoto 6068501, Japan

来源：

JOURNAL OF RADIATION RESEARCH | 2008年 / 49卷 / 02期

关键词：

DNA repair; homologous recombination; nuclear foci; non-homologous end joining;

D O I：

10.1269/jrr.07130

中图分类号：

Q [生物科学];

学科分类号：

07 ; 0710 ; 09 ;

摘要：

DNA double strand break (DSB) is one of the most critical types of damage which is induced by ionizing radiation. In this review, we summarize current progress in investigations on the function of DSB repair-related proteins. We focused on recent findings in the analysis of the function of proteins such as 53BP1, historic H2AX, Mus81-Eme1, Fanc complex, and UBC13, which are found to be related to homologous recombination repair or to non-homologous end joining. In addition to the function of these proteins in DSB repair, the biological function of nuclear foci formation following DSB induction is discussed.

引用

页码：93 / 103

页数：11

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