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有丝分裂和胞质分裂失败导致的 DNA 损伤。

DNA damage associated with mitosis and cytokinesis failure.

机构信息

Molecular and Cellular Biology Department, The Salk Institute for Biological Studies, La Jolla, CA, USA.

出版信息

Oncogene. 2013 Sep 26;32(39):4593-601. doi: 10.1038/onc.2012.615. Epub 2013 Jan 14.

DOI:10.1038/onc.2012.615
PMID:23318447
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3681845/
Abstract

Mitosis is a highly dynamic process, aimed at separating identical copies of genomic material into two daughter cells. A failure of the mitotic process generates cells that carry abnormal chromosome numbers. Such cells are predisposed to become tumorigenic upon continuous cell division and thus need to be removed from the population to avoid cancer formation. Cells that fail in mitotic progression indeed activate cell death or cell cycle arrest pathways; however, these mechanisms are not well understood. Growing evidence suggests that the formation of de novo DNA damage during and after mitotic failure is one of the causal factors that initiate those pathways. Here, we analyze several distinct malfunctions during mitosis and cytokinesis that lead to de novo DNA damage generation.

摘要

有丝分裂是一个高度动态的过程,旨在将基因组物质的相同副本分离到两个子细胞中。有丝分裂过程的失败会产生携带异常染色体数目的细胞。这些细胞在连续细胞分裂时容易癌变,因此需要从群体中清除,以避免癌症形成。在有丝分裂过程中失败的细胞确实会激活细胞死亡或细胞周期停滞途径;然而,这些机制尚不清楚。越来越多的证据表明,有丝分裂失败期间和之后新形成的 DNA 损伤是启动这些途径的原因之一。在这里,我们分析了导致新生成 DNA 损伤的几种不同的有丝分裂和胞质分裂过程中的故障。

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本文引用的文献

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Transcriptional consequences of aneuploidy.非整倍体的转录后果。
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Telomere-driven tetraploidization occurs in human cells undergoing crisis and promotes transformation of mouse cells.端粒驱动的四倍体化发生在人类细胞经历危机时,并促进了小鼠细胞的转化。
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