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Base excision repair of ionizing radiation-induced DNA damage in G1 and G2 cell cycle phases

机译:G1和G2细胞周期阶段的电离辐射诱导的DNA损伤的碱基切除修复

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摘要

BackgroundMajor genomic surveillance mechanisms regulated in response to DNA damage exist at the G1/S and G2/M checkpoints. It is presumed that these delays provide time for the repair of damaged DNA. Cells have developed multiple DNA repair pathways to protect themselves from different types of DNA damage. Oxidative DNA damage is processed by the base excision repair (BER) pathway. Little is known about the BER of ionizing radiation-induced DNA damage and putative heterogeneity of BER in the cell cycle context. We measured the activities of three BER enzymes throughout the cell cycle to investigate the cell cycle-specific repair of ionizing radiation-induced DNA damage. We further examined BER activities in G2 arrested human cells after exposure to ionizing radiation.
机译:背景技术在G1 / S和G2 / M检查站中存在响应DNA损伤而受到调节的主要基因组监测机制。据推测,这些延迟为修复受损的DNA提供了时间。细胞已经开发出多种DNA修复途径来保护自己免受不同类型的DNA损伤。氧化性DNA损伤通过碱基切除修复(BER)途径进行处理。关于电离辐射引起的DNA损伤的BER和在细胞周期背景下BER的假定异质性知之甚少。我们测量了整个细胞周期中三种BER酶的活性,以研究电离辐射诱导的DNA损伤的细胞周期特异性修复。在暴露于电离辐射后,我们进一步检查了G2阻滞人类细胞中的BER活性。

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