DNA damage and L1 retrotransposition.

DNA damage and L1 retrotransposition.
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DNA损伤和L1逆转录。

DOI:
10.1155/jbb/2006/37285
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发表时间:
2006
影响因子:
--
通讯作者:
Prak, Eline T. Luning
Prak, Eline T. Luning
中科院分区:
其他
文献类型:
--
作者:
Farkash, Evan A.;Prak, Eline T. Luning

文献摘要

被引文献

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芭芭拉·麦克林托克是第一个提出转座子是基因组不稳定性的来源,遗传毒性应激有助于它们的动员。双链DNA断裂(DSB)的产生是一种严重的遗传毒性应激形式,其威胁基因组的完整性,激活细胞周期检查点,并且在某些情况下导致细胞死亡。将McClintock的压力假说应用于人类,L1反转录转座子,现代人类基因组中最活跃的自主移动的元件,是否被DSB动员?在这里,回顾了转座因子,特别是逆转录转座子,被遗传毒性应激动员的证据。在DSB形成的背景下,L1迁移率可能会受到L1整合底物、DNA修复机制或L1元件本身变化的影响。 审查的结论与讨论的潜在后果的L1动员的遗传毒性压力的设置。
Barbara McClintock was the first to suggest that transposons are a source of genome instability and that genotoxic stress assisted in their mobilization. The generation of double-stranded DNA breaks (DSBs) is a severe form of genotoxic stress that threatens the integrity of the genome, activates cell cycle checkpoints, and, in some cases, causes cell death. Applying McClintock's stress hypothesis to humans, are L1 retrotransposons, the most active autonomous mobile elements in the modern day human genome, mobilized by DSBs? Here, evidence that transposable elements, particularly retrotransposons, are mobilized by genotoxic stress is reviewed. In the setting of DSB formation, L1 mobility may be affected by changes in the substrate for L1 integration, the DNA repair machinery, or the L1 element itself. The review concludes with a discussion of the potential consequences of L1 mobilization in the setting of genotoxic stress.