端粒功能障碍的细胞遗传学分析
Cytogenetic analysis of telomere dysfunction.
作者信息
Multani Asha S, Chang Sandy
机构信息
Department of Genetics, The University of Texas M.D. Anderson Cancer Center, Houston, TX, USA.
出版信息
Methods Mol Biol. 2011;735:139-43. doi: 10.1007/978-1-61779-092-8_13.
Abstract
Dysfunctional telomeres arising either through natural attrition due to telomerase deficiency or by the removal of telomere binding proteins are recognized as double stranded breaks (DSBs). Repair of DSBs is crucial for the maintenance of genome stability. In mammals, DSBs are repaired by either error prone nonhomologous end joining (NHEJ) or error free homologous recombination (HR) and can be visualized as chromosomal fusions.
摘要
由于端粒酶缺乏导致的自然磨损或通过去除端粒结合蛋白而产生的功能失调的端粒被识别为双链断裂（DSB）。双链断裂的修复对于维持基因组稳定性至关重要。在哺乳动物中，双链断裂通过易出错的非同源末端连接（NHEJ）或无错的同源重组（HR）进行修复，并且可以表现为染色体融合。
相似文献
1
Cytogenetic analysis of telomere dysfunction.端粒功能障碍的细胞遗传学分析
Methods Mol Biol. 2011;735:139-43. doi: 10.1007/978-1-61779-092-8_13.
2
Cytogenetic Analysis of Telomere Dysfunction.端粒功能障碍的细胞遗传学分析
Methods Mol Biol. 2017;1587:127-131. doi: 10.1007/978-1-4939-6892-3_12.
3
The function of classical and alternative non-homologous end-joining pathways in the fusion of dysfunctional telomeres.经典和替代性非同源末端连接途径在功能失调端粒融合中的作用。
EMBO J. 2010 Aug 4;29(15):2598-610. doi: 10.1038/emboj.2010.142. Epub 2010 Jun 29.
4
The DNA damage response at dysfunctional telomeres, and at interstitial and subtelomeric DNA double-strand breaks.功能失调的端粒以及染色体间质和亚端粒区域DNA双链断裂处的DNA损伤反应。
Genes Genet Syst. 2018 Jan 20;92(3):135-152. doi: 10.1266/ggs.17-00014. Epub 2017 Nov 22.
5
NHEJ Contributes to the Fast Repair of Radiation-induced DNA Double-strand Breaks at Late Prophase I Telomeres.非同源末端连接有助于在减数第一次分裂前期晚期的端粒处快速修复辐射诱导的DNA双链断裂。
Health Phys. 2018 Jul;115(1):102-107. doi: 10.1097/HP.0000000000000852.
6
53BP1 deficiency combined with telomere dysfunction activates ATR-dependent DNA damage response.53BP1 缺失与端粒功能障碍激活 ATR 依赖性 DNA 损伤反应。
J Cell Biol. 2012 Apr 16;197(2):283-300. doi: 10.1083/jcb.201110124.
7
Subtelomeric regions in mammalian cells are deficient in DNA double-strand break repair.哺乳动物细胞的端粒区域在 DNA 双链断裂修复中存在缺陷。
DNA Repair (Amst). 2011 May 5;10(5):536-44. doi: 10.1016/j.dnarep.2011.03.001. Epub 2011 Apr 3.
8
Single-strand annealing, conservative homologous recombination, nonhomologous DNA end joining, and the cell cycle-dependent repair of DNA double-strand breaks induced by sparsely or densely ionizing radiation.单链退火、保守同源重组、非同源DNA末端连接以及由稀疏或密集电离辐射诱导的DNA双链断裂的细胞周期依赖性修复。
Radiat Res. 2009 Mar;171(3):265-73. doi: 10.1667/RR0784.1.
9
The Mph1 helicase can promote telomere uncapping and premature senescence in budding yeast.Mph1 解旋酶可促进芽殖酵母端粒去帽和过早衰老。
PLoS One. 2012;7(7):e42028. doi: 10.1371/journal.pone.0042028. Epub 2012 Jul 27.
10
Telomere-Internal Double-Strand Breaks Are Repaired by Homologous Recombination and PARP1/Lig3-Dependent End-Joining.端粒内部双链断裂通过同源重组和PARP1/连接酶3依赖性末端连接进行修复。
Cell Rep. 2016 Nov 1;17(6):1646-1656. doi: 10.1016/j.celrep.2016.10.008.
引用本文的文献
1
Pot1 OB-fold mutations unleash telomere instability to initiate tumorigenesis.端粒保护蛋白1 OB折叠结构域突变引发端粒不稳定从而启动肿瘤发生。
Oncogene. 2017 Apr 6;36(14):1939-1951. doi: 10.1038/onc.2016.405. Epub 2016 Nov 21.
2
TRF2-RAP1 is required to protect telomeres from engaging in homologous recombination-mediated deletions and fusions.TRF2-RAP1对于保护端粒避免参与同源重组介导的缺失和融合是必需的。
Nat Commun. 2016 Mar 4;7:10881. doi: 10.1038/ncomms10881.
3
The E3 ubiquitin ligase Rnf8 stabilizes Tpp1 to promote telomere end protection.E3 泛素连接酶 Rnf8 稳定 Tpp1 以促进端粒末端保护。
Nat Struct Mol Biol. 2011 Nov 20;18(12):1400-7. doi: 10.1038/nsmb.2172.
本文引用的文献
1
Centromere or telomere: who is the boss?着丝粒还是端粒：谁才是主宰？
Anticancer Res. 1995 Nov-Dec;15(6B):2549-50.
2
The possibility of latent centromeres and a proposed nomenclature system for total chromosome and whole arm translocations.潜在着丝粒的可能性以及一种针对全染色体和整条臂易位的提议命名系统。
Cytogenet Cell Genet. 1975;15(1):41-9. doi: 10.1159/000130497.
Zotero 插件