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Telomeric replication stress: the beginning and the end for alternative lengthening of telomeres cancers.端粒复制应激:端粒的替代延长与癌症的开始和结束。
Open Biol. 2022 Mar;12(3):220011. doi: 10.1098/rsob.220011. Epub 2022 Mar 9.
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Structure, Maintenance, and Regulation of Nuclear Pore Complexes: The Gatekeepers of the Eukaryotic Genome.核孔复合体的结构、维护和调控:真核基因组的守门员。
Cold Spring Harb Perspect Biol. 2022 Mar 1;14(3):a040691. doi: 10.1101/cshperspect.a040691.
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Chromatin mobility and relocation in DNA repair.染色质的迁移和重定位在 DNA 修复中。
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Rad52 SUMOylation functions as a molecular switch that determines a balance between the Rad51- and Rad59-dependent survivors.Rad52的类泛素化修饰作为一种分子开关,决定了依赖Rad51和依赖Rad59的存活细胞之间的平衡。
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Alternative lengthening of telomeres is not synonymous with mutations in ATRX/DAXX.端粒替代延长与ATRX/DAXX突变并非同义。
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9
A unified alternative telomere-lengthening pathway in yeast survivor cells.酵母存活细胞中统一的替代性端粒延长途径。
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10
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非经典同源重组的两个 HUB 位于端粒上?NPCs 和 APBs

NPCs and APBs: two HUBs of non-canonical homology-based recombination at telomeres?

机构信息

Centro Andaluz de Biologia Molecular y Medicina Regenerativa (CABIMER), Consejo Superior de Investigaciones Cientificas (CSIC), Universidad de Sevilla, Universidad Pablo de Olavide, Seville, Spain.

MAP Laboratory, INSA Lyon, Claude Bernard University UMR5240, Villeurbanne, France.

出版信息

Cell Cycle. 2023 May;22(10):1163-1168. doi: 10.1080/15384101.2023.2206350. Epub 2023 May 1.

DOI:10.1080/15384101.2023.2206350
PMID:37128641
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10193864/
Abstract

Apart from a few rare exceptions, the maintenance of functional telomeres by recombination-based mechanisms is restricted to accidental and/or pathological situations. Originally described in the yeast S. cerevisiae, this mode of telomere repair has gained interest with the discovery of telomerase negative cancers that use alternative lengthening of telomeres (ALT cancer) dependent on homologous recombination. In both yeast and humans, it has been shown that recombination at telomeres is spatially regulated and occurs preferentially at the nuclear pore complexes (NPCs) in yeast and at ALT-associated promyelocytic leukemia nuclear bodies (APBs) in human cells. Here, we discuss the potential relationships between these two membrane-less structures and their role in enabling unconventional recombination pathways.

摘要

除了少数罕见的例外,基于重组的机制来维持功能端粒仅限于偶然和/或病理情况。这种端粒修复模式最初在酵母 S. cerevisiae 中被描述,随着端粒酶阴性癌症的发现,该模式引起了人们的兴趣,这些癌症依赖于同源重组的端粒的非经典延长(ALT 癌症)。在酵母和人类中,已经表明端粒处的重组受到空间调节,并且在酵母中优先发生在核孔复合物 (NPC) 处,在人类细胞中优先发生在 ALT 相关早幼粒细胞白血病核体 (APB) 处。在这里,我们讨论了这两种无膜结构之间的潜在关系及其在使非传统重组途径成为可能方面的作用。