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Depletion of CoREST does not improve the replication of ICP0 null mutant herpes simplex virus type 1.CoREST 缺失并不能提高 ICP0 缺失突变型单纯疱疹病毒 1 的复制。
J Virol. 2010 Apr;84(7):3695-8. doi: 10.1128/JVI.00021-10. Epub 2010 Jan 27.
2
The two functions of herpes simplex virus 1 ICP0, inhibition of silencing by the CoREST/REST/HDAC complex and degradation of PML, are executed in tandem.单纯疱疹病毒1型ICP0的两个功能，即抑制CoREST/REST/HDAC复合物介导的基因沉默以及降解PML，是协同执行的。
J Virol. 2009 Jan;83(1):181-7. doi: 10.1128/JVI.01940-08. Epub 2008 Oct 22.
3
Replication of ICP0-null mutant herpes simplex virus type 1 is restricted by both PML and Sp100.ICP0缺失突变型单纯疱疹病毒1型的复制受到PML和Sp100的双重限制。
J Virol. 2008 Mar;82(6):2661-72. doi: 10.1128/JVI.02308-07. Epub 2007 Dec 26.
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STAT-1- and IRF-3-dependent pathways are not essential for repression of ICP0-null mutant herpes simplex virus type 1 in human fibroblasts.STAT-1和IRF-3依赖的信号通路对于人成纤维细胞中ICP0缺失突变的单纯疱疹病毒1型的抑制并非必需。
J Virol. 2008 Sep;82(17):8871-81. doi: 10.1128/JVI.00613-08. Epub 2008 Jun 25.
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Components of the REST/CoREST/histone deacetylase repressor complex are disrupted, modified, and translocated in HSV-1-infected cells.REST/CoREST/组蛋白去乙酰化酶抑制复合物的组分在单纯疱疹病毒1型感染的细胞中被破坏、修饰并发生易位。
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Cellular Transcriptional Coactivator RanBP10 and Herpes Simplex Virus 1 ICP0 Interact and Synergistically Promote Viral Gene Expression and Replication.细胞转录共激活因子RanBP10与单纯疱疹病毒1型ICP0相互作用并协同促进病毒基因表达和复制。
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The viral ubiquitin ligase ICP0 is neither sufficient nor necessary for degradation of the cellular DNA sensor IFI16 during herpes simplex virus 1 infection.单纯疱疹病毒 1 感染过程中，病毒泛素连接酶 ICP0 既不充分也不必要，无法降解细胞 DNA 传感器 IFI16。
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Evidence that the herpes simplex virus type 1 ICP0 protein does not initiate reactivation from latency in vivo.单纯疱疹病毒1型ICP0蛋白不会在体内引发潜伏病毒再激活的证据。
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Characterization of a nerve growth factor-inducible cellular activity that enhances herpes simplex virus type 1 gene expression and replication of an ICP0 null mutant in cells of neural lineage.一种神经生长因子诱导的细胞活性的特性，该活性可增强单纯疱疹病毒1型基因表达并促进神经谱系细胞中ICP0缺失突变体的复制。
J Virol. 1998 Jul;72(7):5373-82. doi: 10.1128/JVI.72.7.5373-5382.1998.
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Stimulation of the Replication of ICP0-Null Mutant Herpes Simplex Virus 1 and pp71-Deficient Human Cytomegalovirus by Epstein-Barr Virus Tegument Protein BNRF1.爱泼斯坦-巴尔病毒被膜蛋白BNRF1对ICP0缺失型单纯疱疹病毒1型和pp71缺陷型人巨细胞病毒复制的刺激作用
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A 77 Amino Acid Region in the N-Terminal Half of the HSV-1 E3 Ubiquitin Ligase ICP0 Contributes to Counteracting an Established Type 1 Interferon Response.HSV-1 E3 泛素连接酶 ICP0 的 N 端半胱氨酸 77 氨基酸区域有助于拮抗已建立的 1 型干扰素反应。
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Protocol Optimization for the Production of the Non-Cytotoxic JΔNI5 HSV Vector Deficient in Expression of Immediately Early Genes.用于生产缺乏立即早期基因表达的无细胞毒性JΔNI5单纯疱疹病毒载体的方案优化
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Infected cell protein 0 functional domains and their coordination in herpes simplex virus replication.单纯疱疹病毒复制中感染细胞蛋白0的功能结构域及其协同作用
World J Virol. 2016 Feb 12;5(1):1-13. doi: 10.5501/wjv.v5.i1.1.
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KDM1 class flavin-dependent protein lysine demethylases.KDM1类黄素依赖性蛋白质赖氨酸去甲基化酶。
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F-actin bundles direct the initiation and orientation of lamellipodia through adhesion-based signaling.F-肌动蛋白束通过基于黏附的信号传导来指导片状伪足的起始和定向。
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The molecular basis of herpes simplex virus latency.单纯疱疹病毒潜伏的分子基础。
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HSV-1 ICP0: paving the way for viral replication.单纯疱疹病毒1型感染细胞蛋白0：为病毒复制铺平道路。
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9
Herpes simplex virus immediate-early protein ICP0 is targeted by SIAH-1 for proteasomal degradation.单纯疱疹病毒立即早期蛋白 ICP0 被 SIAH-1 靶向进行蛋白酶体降解。
J Virol. 2011 Aug;85(15):7644-57. doi: 10.1128/JVI.02207-10. Epub 2011 Jun 1.
10
Activities of ICP0 involved in the reversal of silencing of quiescent herpes simplex virus 1.ICP0 参与逆转潜伏的单纯疱疹病毒 1 的沉默。
J Virol. 2011 May;85(10):4993-5002. doi: 10.1128/JVI.02265-10. Epub 2011 Mar 16.

本文引用的文献

1
Regulation of ICP0-null mutant herpes simplex virus type 1 infection by ND10 components ATRX and hDaxx.ICP0 缺失突变单纯疱疹病毒 1 感染的调控因子：ATRX 和 hDaxx。
J Virol. 2010 Apr;84(8):4026-40. doi: 10.1128/JVI.02597-09. Epub 2010 Feb 10.
2
Analysis of the functions of herpes simplex virus type 1 regulatory protein ICP0 that are critical for lytic infection and derepression of quiescent viral genomes.对单纯疱疹病毒1型调节蛋白ICP0功能的分析，这些功能对于裂解感染和静止病毒基因组的去抑制至关重要。
J Virol. 2009 May;83(10):4963-77. doi: 10.1128/JVI.02593-08. Epub 2009 Mar 4.
3
Herpes simplex virus type 1 regulatory protein ICP0 aids infection in cells with a preinduced interferon response but does not impede interferon-induced gene induction.单纯疱疹病毒1型调节蛋白ICP0有助于在具有预先诱导的干扰素反应的细胞中感染，但不妨碍干扰素诱导的基因诱导。
J Virol. 2009 May;83(10):4978-83. doi: 10.1128/JVI.02595-08. Epub 2009 Mar 4.
4
Components of nuclear domain 10 bodies regulate varicella-zoster virus replication.核结构域10小体的组成成分调控水痘-带状疱疹病毒复制。
J Virol. 2009 May;83(9):4262-74. doi: 10.1128/JVI.00021-09. Epub 2009 Feb 11.
5
Engagement of the lysine-specific demethylase/HDAC1/CoREST/REST complex by herpes simplex virus 1.单纯疱疹病毒1对赖氨酸特异性去甲基化酶/组蛋白去乙酰化酶1/CoREST/REST复合物的作用
J Virol. 2009 May;83(9):4376-85. doi: 10.1128/JVI.02515-08. Epub 2009 Feb 4.
6
The two functions of herpes simplex virus 1 ICP0, inhibition of silencing by the CoREST/REST/HDAC complex and degradation of PML, are executed in tandem.单纯疱疹病毒1型ICP0的两个功能，即抑制CoREST/REST/HDAC复合物介导的基因沉默以及降解PML，是协同执行的。
J Virol. 2009 Jan;83(1):181-7. doi: 10.1128/JVI.01940-08. Epub 2008 Oct 22.
7
STAT-1- and IRF-3-dependent pathways are not essential for repression of ICP0-null mutant herpes simplex virus type 1 in human fibroblasts.STAT-1和IRF-3依赖的信号通路对于人成纤维细胞中ICP0缺失突变的单纯疱疹病毒1型的抑制并非必需。
J Virol. 2008 Sep;82(17):8871-81. doi: 10.1128/JVI.00613-08. Epub 2008 Jun 25.
8
Replication of ICP0-null mutant herpes simplex virus type 1 is restricted by both PML and Sp100.ICP0缺失突变型单纯疱疹病毒1型的复制受到PML和Sp100的双重限制。
J Virol. 2008 Mar;82(6):2661-72. doi: 10.1128/JVI.02308-07. Epub 2007 Dec 26.
9
Herpes simplex virus-infected cell protein 0 blocks the silencing of viral DNA by dissociating histone deacetylases from the CoREST-REST complex.单纯疱疹病毒感染细胞蛋白0通过使组蛋白脱乙酰酶与CoREST-REST复合物解离来阻断病毒DNA的沉默。
Proc Natl Acad Sci U S A. 2007 Oct 23;104(43):17134-9. doi: 10.1073/pnas.0707266104. Epub 2007 Oct 15.
10
Evidence that the herpes simplex virus type 1 ICP0 protein does not initiate reactivation from latency in vivo.单纯疱疹病毒1型ICP0蛋白不会在体内引发潜伏病毒再激活的证据。
J Virol. 2006 Nov;80(22):10919-30. doi: 10.1128/JVI.01253-06. Epub 2006 Aug 30.

CoREST 缺失并不能提高 ICP0 缺失突变型单纯疱疹病毒 1 的复制。

Depletion of CoREST does not improve the replication of ICP0 null mutant herpes simplex virus type 1.

机构信息

MRC Virology Unit, Institute of Virology, Church Street, Glasgow G11 5JR, Scotland, United Kingdom.

出版信息

J Virol. 2010 Apr;84(7):3695-8. doi: 10.1128/JVI.00021-10. Epub 2010 Jan 27.

DOI:10.1128/JVI.00021-10
PMID:20106915
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2838130/
Abstract

It has been proposed that the cellular corepressor protein CoREST is involved in repressing herpes simplex virus type 1 (HSV-1) infection in the absence of the viral regulatory protein ICP0. This proposal predicts that depletion of CoREST should improve the plaque-forming efficiency and replication of ICP0 null mutant virus. To test this hypothesis, human HepaRG cells that were highly depleted of CoREST were isolated using RNA interference technology. Depletion of CoREST had no effect on the replication of ICP0 null mutant HSV-1, demonstrating that CoREST does not play an influential role in regulating HSV-1 infection in this cell type.

摘要

有人提出，细胞核心抑制蛋白 CoREST 参与在没有病毒调节蛋白 ICP0 的情况下抑制单纯疱疹病毒 1 型（HSV-1）的感染。这一假说预测，CoREST 的耗竭应该会提高 ICP0 缺失突变病毒的噬菌斑形成效率和复制。为了验证这一假设，使用 RNA 干扰技术从 HepaRG 细胞中高度耗竭 CoREST 以分离细胞。CoREST 的耗竭对 ICP0 缺失突变 HSV-1 的复制没有影响，表明 CoREST 在这种细胞类型中对调节 HSV-1 感染不起重要作用。