Repair of Accidental DNA Double-Strand Breaks in the Human Genome and Its Relevance to Vector DNA Integration
Repair of Accidental DNA Double-Strand Breaks in the Human Genome and Its Relevance to Vector DNA Integration
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DOI：
10.4172/2329-6682.1000e107
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发表时间：
2014
期刊：
影响因子：
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通讯作者：
N. Adachi;Shinta Saito;Aya Kurosawa
中科院分区：
文献类型：
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作者：
N. Adachi;Shinta Saito;Aya Kurosawa
染色体DNA损伤的有效修复是细胞维持基因组完整性的关键。DNA双链断裂(DSB)是最严重的DNA损伤类型，可由各种外源性和内源性机制引起，如电离辐射、活性氧、拓扑异构酶毒物或复制错误[1]。如果不修复或错误修复DSB，会导致细胞死亡或染色体异常[2，3]。人类细胞已经进化出两种根本不同的修复染色体DSB的机制，同源重组(HR)和非同源末端连接(NHEJ)[4]。NHEJ不仅修复意外的(非生理性)DSB，而且对于在B和T淋巴细胞V(D)J重组和成熟B细胞的类开关重组过程中出现的生理性DSB的重新连接也是必不可少的[3]。
Efficient repair of chromosomal DNA damage is crucial for cells to maintain genome integrity. DNA double-strand breaks (DSBs) are the most severe type of DNA lesions that can be caused by various exogenous and endogenous mechanisms, such as ionizing radiation, reactive oxygen species, topoisomerase poisons, or replication errors [1]. DSBs, if left unrepaired or mis-repaired, lead to cell death or chromosomal aberrations [2,3]. Human cells have evolved two fundamentally different mechanisms for repairing chromosomal DSBs, homologous recombination (HR) and non-homologous end-joining (NHEJ) [4]. NHEJ not only repairs accidental (non-physiological) DSBs, but is also essential for rejoining physiological DSBs that arise in the process of V(D)J recombination in B and T lymphocytes and class switch recombination in mature B cells [3].