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将异常有丝分裂与 DNA 损伤的获得联系起来。

Linking abnormal mitosis to the acquisition of DNA damage.

机构信息

Howard Hughes Medical Institute, Department of Pediatric Oncology, Dana-Farber Cancer Institute, Children's Hospital, Department of Cell Biology, Harvard Medical School, Boston, MA 02115, USA.

出版信息

J Cell Biol. 2012 Dec 10;199(6):871-81. doi: 10.1083/jcb.201210040.

DOI:10.1083/jcb.201210040
PMID:23229895
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3518222/
Abstract

Cellular defects that impair the fidelity of mitosis promote chromosome missegregation and aneuploidy. Increasing evidence reveals that errors in mitosis can also promote the direct and indirect acquisition of DNA damage and chromosome breaks. Consequently, deregulated cell division can devastate the integrity of the normal genome and unleash a variety of oncogenic stimuli that may promote transformation. Recent work has shed light on the mechanisms that link abnormal mitosis with the development of DNA damage, how cells respond to such affronts, and the potential impact on tumorigenesis.

摘要

细胞缺陷会损害有丝分裂的保真度,从而促进染色体错分和非整倍体。越来越多的证据表明,有丝分裂中的错误也可以促进 DNA 损伤和染色体断裂的直接和间接获得。因此,细胞分裂失控会破坏正常基因组的完整性,并释放出各种可能促进转化的致癌刺激物。最近的研究揭示了将异常有丝分裂与 DNA 损伤的发展联系起来的机制,细胞如何应对这些挑战,以及对肿瘤发生的潜在影响。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4d14/3518222/3d2c7783c02f/JCB_201210040_Fig3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4d14/3518222/1bb162b1cef3/JCB_201210040_Fig1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4d14/3518222/0fa749af27f6/JCB_201210040_Fig2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4d14/3518222/3d2c7783c02f/JCB_201210040_Fig3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4d14/3518222/1bb162b1cef3/JCB_201210040_Fig1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4d14/3518222/0fa749af27f6/JCB_201210040_Fig2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4d14/3518222/3d2c7783c02f/JCB_201210040_Fig3.jpg

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Global analysis of genome, transcriptome and proteome reveals the response to aneuploidy in human cells.对基因组、转录组和蛋白质组的全面分析揭示了人类细胞对非整倍体的反应。
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GF-15, a novel inhibitor of centrosomal clustering, suppresses tumor cell growth in vitro and in vivo.GF-15,一种新型的中心体聚类抑制剂,在体外和体内抑制肿瘤细胞生长。
耐药前列腺癌细胞的单细胞蛋白质组学表征揭示与形态变化相关的分子特征。
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Increased DNA damage in full-grown oocytes is correlated with diminished autophagy activation.成熟卵母细胞中 DNA 损伤的增加与自噬激活的减弱有关。
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