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Timeless-dependent DNA replication-coupled recombination promotes Kaposi's Sarcoma-associated herpesvirus episome maintenance and terminal repeat stability.时空调控的 DNA 复制偶联重组促进卡波西肉瘤相关疱疹病毒的病毒体维持和末端重复稳定性。
J Virol. 2013 Apr;87(7):3699-709. doi: 10.1128/JVI.02211-12. Epub 2013 Jan 16.
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Two faces of brd4: mitotic bookmark and transcriptional lynchpin.BRD4的两面性:有丝分裂书签与转录关键因子
Transcription. 2013 Jan-Feb;4(1):13-7. doi: 10.4161/trns.22542. Epub 2012 Nov 6.
3
Phosphorylation of the chromatin binding domain of KSHV LANA.磷酸化 KSHV LANA 的染色质结合域。
PLoS Pathog. 2012;8(10):e1002972. doi: 10.1371/journal.ppat.1002972. Epub 2012 Oct 18.
4
Genome-wide analyses of Zta binding to the Epstein-Barr virus genome reveals interactions in both early and late lytic cycles and an epigenetic switch leading to an altered binding profile.全基因组分析 Zta 与 EBV 基因组的结合揭示了在早期和晚期裂解周期中的相互作用,以及导致结合谱改变的表观遗传开关。
J Virol. 2012 Dec;86(23):12494-502. doi: 10.1128/JVI.01705-12. Epub 2012 Sep 26.
5
An atlas of the Epstein-Barr virus transcriptome and epigenome reveals host-virus regulatory interactions.《爱泼斯坦-巴尔病毒转录组和表观基因组图谱揭示了宿主-病毒的调控相互作用》
Cell Host Microbe. 2012 Aug 16;12(2):233-45. doi: 10.1016/j.chom.2012.06.008.
6
Cancer epigenetics: from mechanism to therapy.癌症表观遗传学:从机制到治疗。
Cell. 2012 Jul 6;150(1):12-27. doi: 10.1016/j.cell.2012.06.013.
7
Kaposi's sarcoma-associated herpesvirus-encoded LANA recruits topoisomerase IIβ for latent DNA replication of the terminal repeats.卡波西肉瘤相关疱疹病毒编码的 LANA 招募拓扑异构酶 IIβ 用于末端重复序列的潜伏 DNA 复制。
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Cohesins repress Kaposi's sarcoma-associated herpesvirus immediate early gene transcription during latency.黏连蛋白在潜伏期间抑制卡波西肉瘤相关疱疹病毒即刻早期基因转录。
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9
The bromodomain interaction module.溴结构域相互作用模块。
FEBS Lett. 2012 Aug 14;586(17):2692-704. doi: 10.1016/j.febslet.2012.04.045. Epub 2012 May 3.
10
The ubiquitin-specific protease USP7 modulates the replication of Kaposi's sarcoma-associated herpesvirus latent episomal DNA.泛素特异性蛋白酶 USP7 调节卡波西肉瘤相关疱疹病毒潜伏性 episomal DNA 的复制。
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EBV 和 KSHV 潜伏期的表观遗传调控。

Epigenetic regulation of EBV and KSHV latency.

机构信息

The Wistar Institute, Philadelphia, PA 19104, United States.

出版信息

Curr Opin Virol. 2013 Jun;3(3):251-9. doi: 10.1016/j.coviro.2013.03.004. Epub 2013 Apr 16.

DOI:10.1016/j.coviro.2013.03.004
PMID:23601957
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3947873/
Abstract

The gammaherpesviruses are unique for their capacity to establish a variety of gene expression programs during latent and lytic infection. This capacity enables the virus to control host-cell proliferation, prevent programmed cell death, elude immune cell detection, and ultimately adapt to a wide range of environmental and developmental changes in the host cell. This remarkable plasticity of gene expression results from the combined functionalities of viral and host factors that biochemically remodel and epigenetically modify the viral chromosome. These epigenetic modifications range from primary DNA methylations, to chromatin protein post-translational modifications, to higher-order chromosome conformations. In addition, gammaherpesviruses have acquired specialized tools to modulate the epigenetic processes that promote viral genome propagation and host-cell survival.

摘要

γ疱疹病毒的独特之处在于其在潜伏和裂解感染期间能够建立多种基因表达程序。这种能力使病毒能够控制宿主细胞的增殖、防止程序性细胞死亡、逃避免疫细胞的检测,并最终适应宿主细胞中广泛的环境和发育变化。这种基因表达的显著可塑性源于病毒和宿主因子的共同功能,这些因子通过生化重塑和表观遗传修饰病毒染色体。这些表观遗传修饰包括初级 DNA 甲基化、染色质蛋白翻译后修饰以及高级染色体构象。此外,γ疱疹病毒还获得了专门的工具来调节促进病毒基因组复制和宿主细胞存活的表观遗传过程。