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本文引用的文献

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Sirtuins as regulators of metabolism and healthspan.沉默调节蛋白作为代谢和寿命的调节剂。
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The sirtuin SIRT6 regulates lifespan in male mice.SIRT6 蛋白去乙酰化酶调控雄性小鼠寿命。
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RSC facilitates Rad59-dependent homologous recombination between sister chromatids by promoting cohesin loading at DNA double-strand breaks.RSC 通过促进黏连蛋白在 DNA 双链断裂处的加载,促进姐妹染色单体之间 Rad59 依赖性同源重组。
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Histone demethylase UTX-1 regulates C. elegans life span by targeting the insulin/IGF-1 signaling pathway.组蛋白去甲基酶 UTX-1 通过靶向胰岛素/IGF-1 信号通路来调节秀丽隐杆线虫的寿命。
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Histone H4 lysine 16 hypoacetylation is associated with defective DNA repair and premature senescence in Zmpste24-deficient mice.组蛋白 H4 赖氨酸 16 低乙酰化与 Zmpste24 缺陷小鼠中 DNA 修复缺陷和过早衰老有关。
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BMI1 is recruited to DNA breaks and contributes to DNA damage-induced H2A ubiquitination and repair.BMI1 被招募到 DNA 断裂处,并有助于 DNA 损伤诱导的 H2A 泛素化和修复。
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ATP-dependent chromatin remodeling: genetics, genomics and mechanisms.ATP 依赖的染色质重塑:遗传学、基因组学和机制。
Cell Res. 2011 Mar;21(3):396-420. doi: 10.1038/cr.2011.32. Epub 2011 Mar 1.
8
Interplay between oncogene-induced DNA damage response and heterochromatin in senescence and cancer.癌基因诱导的 DNA 损伤反应与衰老和癌症中的异染色质之间的相互作用。
Nat Cell Biol. 2011 Mar;13(3):292-302. doi: 10.1038/ncb2170. Epub 2011 Feb 20.
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The 53BP1-EXPAND1 connection in chromatin structure regulation.染色质结构调控中的 53BP1-EXPAND1 连接。
Nucleus. 2010 Nov-Dec;1(6):472-4. doi: 10.4161/nucl.1.6.13059. Epub 2010 Jul 18.
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MMSET regulates histone H4K20 methylation and 53BP1 accumulation at DNA damage sites.MMSET 调控组蛋白 H4K20 甲基化和 53BP1 在 DNA 损伤部位的积累。
Nature. 2011 Feb 3;470(7332):124-8. doi: 10.1038/nature09658.

染色质重塑、DNA 损伤修复与衰老。

Chromatin remodeling, DNA damage repair and aging.

机构信息

Shenzhen Institute of Research and Innovation, The University of Hong Kong, Shenzhen, China ; Department of Biochemistry, LKS Faculty of Medicine, The University of Hong Kong, Hong Kong.

出版信息

Curr Genomics. 2012 Nov;13(7):533-47. doi: 10.2174/138920212803251373.

DOI:10.2174/138920212803251373
PMID:23633913
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3468886/
Abstract

Cells are constantly exposed to a variety of environmental and endogenous conditions causing DNA damage, which is detected and repaired by conserved DNA repair pathways to maintain genomic integrity. Chromatin remodeling is critical in this process, as the organization of eukaryotic DNA into compact chromatin presents a natural barrier to all DNA-related events. Studies on human premature aging syndromes together with normal aging have suggested that accumulated damages might lead to exhaustion of resources that are required for physiological functions and thus accelerate aging. In this manuscript, combining the present understandings and latest findings, we focus mainly on discussing the role of chromatin remodeling in the repair of DNA double-strand breaks (DSBs) and regulation of aging.

摘要

细胞不断受到各种环境和内源性条件的影响,导致 DNA 损伤,这些损伤可被保守的 DNA 修复途径检测和修复,以维持基因组的完整性。染色质重塑在这个过程中至关重要,因为真核生物 DNA 组织成致密的染色质,这对所有与 DNA 相关的事件构成了天然的障碍。对人类早衰综合征和正常衰老的研究表明,积累的损伤可能导致生理功能所需资源的耗尽,从而加速衰老。在本文中,结合目前的认识和最新的发现,我们主要讨论了染色质重塑在修复 DNA 双链断裂(DSBs)和调节衰老中的作用。