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本文引用的文献

1
Epigenetics of latent Epstein-Barr virus genomes: high resolution methylation analysis of the bidirectional promoter region of latent membrane protein 1 and 2B genes.
Biol Chem. 2001 Apr;382(4):699-705. doi: 10.1515/BC.2001.083.
2
Regulation of the Epstein-Barr virus C promoter by AUF1 and the cyclic AMP/protein kinase A signaling pathway.AUF1和环磷酸腺苷/蛋白激酶A信号通路对爱泼斯坦-巴尔病毒C启动子的调控
J Virol. 2000 Sep;74(17):8166-75. doi: 10.1128/jvi.74.17.8166-8175.2000.
3
Epstein-barr virus nuclear antigen 3C activates the latent membrane protein 1 promoter in the presence of Epstein-Barr virus nuclear antigen 2 through sequences encompassing an spi-1/Spi-B binding site.爱泼斯坦-巴尔病毒核抗原3C在爱泼斯坦-巴尔病毒核抗原2存在的情况下,通过包含一个spi-1/Spi-B结合位点的序列激活潜伏膜蛋白1启动子。
J Virol. 2000 Jun;74(11):5151-60. doi: 10.1128/jvi.74.11.5151-5160.2000.
4
De novo DNA methylation at nonrandom founder sites 5' from an unmethylated minimal origin of DNA replication in latent Epstein-Barr virus genomes.在潜伏的爱泼斯坦-巴尔病毒基因组中,未甲基化的最小DNA复制起点上游5'处的非随机起始位点发生从头DNA甲基化。
Biol Chem. 2000 Feb;381(2):95-105. doi: 10.1515/BC.2000.014.
5
Modulation of DNA binding protein affinity directly affects target site demethylation.DNA结合蛋白亲和力的调节直接影响靶位点去甲基化。
Mol Cell Biol. 2000 Apr;20(7):2343-9. doi: 10.1128/MCB.20.7.2343-2349.2000.
6
A role for SKIP in EBNA2 activation of CBF1-repressed promoters.SKIP在EBNA2激活CBF1抑制的启动子中的作用。
J Virol. 2000 Feb;74(4):1939-47. doi: 10.1128/jvi.74.4.1939-1947.2000.
7
DNA methylation de novo.DNA 从头甲基化
Science. 1999 Dec 17;286(5448):2287-8. doi: 10.1126/science.286.5448.2287.
8
Differential methylation of Epstein-Barr virus latency promoters facilitates viral persistence in healthy seropositive individuals.爱泼斯坦-巴尔病毒潜伏启动子的差异甲基化促进病毒在健康血清阳性个体中的持续存在。
J Virol. 1999 Dec;73(12):9959-68. doi: 10.1128/JVI.73.12.9959-9968.1999.
9
Repression of Epstein-Barr virus EBNA-1 gene transcription by pRb during restricted latency.在受限潜伏期期间,pRb对爱泼斯坦-巴尔病毒EBNA-1基因转录的抑制作用
J Virol. 1999 Oct;73(10):7943-51. doi: 10.1128/JVI.73.10.7943-7951.1999.
10
Methylation status of the Epstein-Barr virus major latent promoter C in iatrogenic B cell lymphoproliferative disease. Application of PCR-based analysis.医源性B细胞淋巴增殖性疾病中EB病毒主要潜伏启动子C的甲基化状态。基于聚合酶链反应分析的应用。
Am J Pathol. 1999 Aug;155(2):619-25. doi: 10.1016/S0002-9440(10)65157-7.

爱泼斯坦-巴尔病毒潜伏相关启动子Qp、Cp和LMP1p在核苷酸分辨率下的蛋白质-DNA结合及CpG甲基化

Protein-DNA binding and CpG methylation at nucleotide resolution of latency-associated promoters Qp, Cp, and LMP1p of Epstein-Barr virus.

作者信息

Salamon D, Takacs M, Ujvari D, Uhlig J, Wolf H, Minarovits J, Niller H H

机构信息

Microbiological Research Group, National Center for Epidemiology, H-1529 Budapest, Hungary.

出版信息

J Virol. 2001 Mar;75(6):2584-96. doi: 10.1128/JVI.75.6.2584-2596.2001.

DOI:10.1128/JVI.75.6.2584-2596.2001
PMID:11222681
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC115881/
Abstract

Epstein-Barr viral (EBV) latency-associated promoters Qp, Cp, and LMP1p are crucial for the regulated expression of the EBNA and LMP transcripts in dependence of the latency type. By transient transfection and in vitro binding analyses, many promoter elements and transcription factors have previously been shown to be involved in the activities of these promoters. However, the latency promoters have only partially been examined at the nucleotide level in vivo. Therefore, we undertook a comprehensive analysis of in vivo protein binding and CpG methylation patterns at these promoters in five representative cell lines and correlated the results with the known in vitro binding data and activities of these promoters from previous transfection experiments. Promoter activity inversely correlated with the methylation state of promoters, although Qp was a remarkable exception. Novel protein binding data were obtained for all promoters. For Cp, binding correlated well with promoter activity; for LMP1p and Qp, binding patterns looked similar regardless of promoter activity.

摘要

爱泼斯坦-巴尔病毒(EBV)潜伏相关启动子Qp、Cp和LMP1p对于根据潜伏类型调控EBNA和LMP转录本的表达至关重要。通过瞬时转染和体外结合分析,先前已表明许多启动子元件和转录因子参与这些启动子的活性。然而,潜伏启动子在体内核苷酸水平上仅得到了部分研究。因此,我们对五种代表性细胞系中这些启动子的体内蛋白质结合和CpG甲基化模式进行了全面分析,并将结果与先前转染实验中已知的体外结合数据和这些启动子的活性相关联。启动子活性与启动子的甲基化状态呈负相关,尽管Qp是一个显著的例外。所有启动子均获得了新的蛋白质结合数据。对于Cp,结合与启动子活性密切相关;对于LMP1p和Qp,无论启动子活性如何,结合模式看起来相似。