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DNA non-homologous end-joining enters the resection arena.

作者信息

Jeggo Penny A, Löbrich Markus

机构信息

Markus Löbrich: Darmstadt University of Technology, Radiation Biology and DNA Repair, Darmstadt, Germany.

出版信息

Oncotarget. 2017 Oct 26;8(55):93317-93318. doi: 10.18632/oncotarget.22075. eCollection 2017 Nov 7.

DOI:10.18632/oncotarget.22075
PMID:29212151
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5706797/
Abstract
摘要

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DNA non-homologous end-joining enters the resection arena.DNA非同源末端连接进入了切除领域。
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2
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4
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本文引用的文献

1
A Process of Resection-Dependent Nonhomologous End Joining Involving the Goddess Artemis.一种涉及Artemis蛋白的依赖切除的非同源末端连接过程。
Trends Biochem Sci. 2017 Sep;42(9):690-701. doi: 10.1016/j.tibs.2017.06.011. Epub 2017 Jul 21.
2
DNA Double-Strand Break Resection Occurs during Non-homologous End Joining in G1 but Is Distinct from Resection during Homologous Recombination.DNA双链断裂切除在G1期的非同源末端连接过程中发生，但与同源重组过程中的切除不同。
Mol Cell. 2017 Feb 16;65(4):671-684.e5. doi: 10.1016/j.molcel.2016.12.016. Epub 2017 Jan 26.
3
Mechanism and regulation of DNA end resection in eukaryotes.真核生物中DNA末端切除的机制与调控
Crit Rev Biochem Mol Biol. 2016 May-Jun;51(3):195-212. doi: 10.3109/10409238.2016.1172552. Epub 2016 Apr 20.
4
Alternative end-joining repair pathways are the ultimate backup for abrogated classical non-homologous end-joining and homologous recombination repair: Implications for the formation of chromosome translocations.替代末端连接修复途径是经典非同源末端连接和同源重组修复被废除后的最终备用途径：对染色体易位形成的影响。
Mutat Res Genet Toxicol Environ Mutagen. 2015 Nov;793:166-75. doi: 10.1016/j.mrgentox.2015.07.001. Epub 2015 Jul 4.
5
Polo-like kinase 3 regulates CtIP during DNA double-strand break repair in G1.Polo样激酶3在G1期DNA双链断裂修复过程中调控CtIP。
J Cell Biol. 2014 Sep 29;206(7):877-94. doi: 10.1083/jcb.201401146.
6
Site-specific DICER and DROSHA RNA products control the DNA-damage response.靶向 DICER 和 DROSHA 的 RNA 产物可控制 DNA 损伤反应。
Nature. 2012 Aug 9;488(7410):231-5. doi: 10.1038/nature11179.
7
ATM and Artemis promote homologous recombination of radiation-induced DNA double-strand breaks in G2.ATM和Artemis促进G2期辐射诱导的DNA双链断裂的同源重组。
EMBO J. 2009 Nov 4;28(21):3413-27. doi: 10.1038/emboj.2009.276. Epub 2009 Sep 24.
8
A pathway of double-strand break rejoining dependent upon ATM, Artemis, and proteins locating to gamma-H2AX foci.一条依赖于ATM、Artemis以及定位于γ-H2AX病灶的蛋白质的双链断裂重新连接途径。
Mol Cell. 2004 Dec 3;16(5):715-24. doi: 10.1016/j.molcel.2004.10.029.