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Mol Cell Oncol. 2015 Jul 6;3(1):e1063571. doi: 10.1080/23723556.2015.1063571. eCollection 2016 Jan.
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Nuclear deubiquitination in the spotlight: the multifaceted nature of USP7 biology in disease.核去泛素化备受关注:USP7 生物学在疾病中的多面性。
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本文引用的文献

1
USP7 is essential for maintaining Rad18 stability and DNA damage tolerance.USP7对于维持Rad18稳定性和DNA损伤耐受性至关重要。
Oncogene. 2016 Feb 25;35(8):965-76. doi: 10.1038/onc.2015.149. Epub 2015 May 11.
2
DNA damage-specific deubiquitination regulates Rad18 functions to suppress mutagenesis.DNA 损伤特异性去泛素化调节 Rad18 功能以抑制诱变。
J Cell Biol. 2014 Jul 21;206(2):183-97. doi: 10.1083/jcb.201311063. Epub 2014 Jul 14.
3
Competition, collaboration and coordination--determining how cells bypass DNA damage.竞争、合作与协调——决定细胞如何绕过 DNA 损伤。
J Cell Sci. 2012 Apr 1;125(Pt 7):1633-43. doi: 10.1242/jcs.094748. Epub 2012 Apr 12.
4
M phase phosphorylation of the epigenetic regulator UHRF1 regulates its physical association with the deubiquitylase USP7 and stability.M 期磷酸化的表观遗传调控因子 UHRF1 调节其与去泛素化酶 USP7 的物理结合及其稳定性。
Proc Natl Acad Sci U S A. 2012 Mar 27;109(13):4828-33. doi: 10.1073/pnas.1116349109. Epub 2012 Mar 12.
5
Elevated expression of Rad18 regulates melanoma cell proliferation.Rad18 表达水平升高可调节黑素瘤细胞增殖。
Pigment Cell Melanoma Res. 2012 Mar;25(2):213-8. doi: 10.1111/j.1755-148X.2011.00948.x. Epub 2012 Jan 12.
6
The auto-ubiquitylation of E3 ubiquitin-protein ligase Chfr at G2 phase is required for accumulation of polo-like kinase 1 and mitotic entry in mammalian cells.E3 泛素连接酶 Chfr 在 G2 期的自身泛素化对于哺乳动物细胞中 polo 样激酶 1 的积累和有丝分裂进入是必需的。
J Biol Chem. 2011 Sep 2;286(35):30615-30623. doi: 10.1074/jbc.M111.231803. Epub 2011 Jul 15.
7
The multifaceted roles of USP7: new therapeutic opportunities.USP7 的多效性作用:新的治疗机会。
Cell Biochem Biophys. 2011 Jun;60(1-2):61-8. doi: 10.1007/s12013-011-9185-5.
8
Molecular recognition of p53 and MDM2 by USP7/HAUSP.USP7/HAUSP对p53和MDM2的分子识别
Nat Struct Mol Biol. 2006 Mar;13(3):285-91. doi: 10.1038/nsmb1067. Epub 2006 Feb 12.
9
Regulated expression and dynamic changes in subnuclear localization of mammalian Rad18 under normal and genotoxic conditions.
Genes Cells. 2005 Aug;10(8):753-62. doi: 10.1111/j.1365-2443.2005.00874.x.
10
Differential regulation of Rad18 through Rad6-dependent mono- and polyubiquitination.通过Rad6依赖的单泛素化和多泛素化对Rad18进行差异调控。
J Biol Chem. 2005 Jan 7;280(1):515-24. doi: 10.1074/jbc.M409219200. Epub 2004 Oct 27.

受损的复制叉耐受USP7以维持基因组稳定性。

Damaged replication forks tolerate USP7 to maintain genome stability.

作者信息

Zlatanou Anastasia, Stewart Grant S

机构信息

School of Cancer Sciences, University of Birmingham , Birmingham, UK.

出版信息

Mol Cell Oncol. 2015 Jul 6;3(1):e1063571. doi: 10.1080/23723556.2015.1063571. eCollection 2016 Jan.

DOI:10.1080/23723556.2015.1063571
PMID:27308573
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4845244/
Abstract

RAD18 functions to promote DNA damage tolerance (DTT), a process that ensures faithful genome duplication. Protein ubiquitylation/deubiquitylation is a critical regulatory mechanism controlling DTT. Recently, we have identified the deubiquitylating enzyme USP7 as a component of the DTT machinery that acts to protect RAD18 from proteasome-dependent degradation.

摘要

RAD18的功能是促进DNA损伤耐受(DTT),这是一个确保基因组忠实复制的过程。蛋白质泛素化/去泛素化是控制DTT的关键调节机制。最近,我们鉴定出去泛素化酶USP7是DTT机制的一个组成部分,其作用是保护RAD18免受蛋白酶体依赖性降解。