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首页> 外文期刊>Cell cycle >A novel role for Chk2 after DNA damage in mitosis?
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A novel role for Chk2 after DNA damage in mitosis?

机译：DNA损伤后有丝分裂中Chk2的新作用？

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摘要

The activation of the DNA damage response pathway in human somatic cells involves the checkpoint kinases ATM/ATR, Chk1, Chk2 as well as the tumor suppressor and transcription factor p53 and results in a cell cycle arrest at G_1/S or G_2/M depending on the stage when the DNA damage occurred. In contrast to mammalian cells, Drosophila embryonic cells do not arrest at the G_2/M transition in response to unreplicated DNA or DNA damage, but instead exhibit a delay in mitosis, which is caused by centrosome inactivation associated with spindle formation defects. In this animal system it has been shown that the centrosome disruption is dependent on the Chk2 kinase and might represent a mechanism to facilitate cell death when cells enter mitosis in the presence of DNA damage, often referred to as mitotic catastrophe. Similarly, in mammalian cells the centrosome integrity is impaired upon DNA damage in mitosis, resulting in chromosome missegregation and eventually in cell death.
机译：人类体细胞中DNA损伤应答途径的激活涉及检查点激酶ATM / ATR，Chk1，Chk2以及肿瘤抑制因子和转录因子p53，并导致细胞周期停滞在G_1 / S或G_2 / M，具体取决于DNA损伤发生的阶段。与哺乳动物细胞相比，果蝇胚胎细胞不响应未复制的DNA或DNA损伤而停滞在G_2 / M转变，而是表现出有丝分裂的延迟，这是由与纺锤体形成缺陷相关的中心体失活引起的。在该动物系统中，已经证明，中心体破坏取决于Chk2激酶，并且可能代表一种机制，当细胞在存在DNA损伤（通常称为有丝分裂灾难）的情况下进入有丝分裂时，有助于细胞死亡。同样，在哺乳动物细胞中，有丝分裂中的DNA损伤会损害中心体的完整性，从而导致染色体错聚并最终导致细胞死亡。

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