• 文献检索
  • 文档翻译
  • 深度研究
  • 学术资讯
  • Suppr Zotero 插件Zotero 插件
  • 邀请有礼
  • 套餐&价格
  • 历史记录
应用&插件
Suppr Zotero 插件Zotero 插件浏览器插件Mac 客户端Windows 客户端微信小程序
定价
高级版会员购买积分包购买API积分包
服务
文献检索文档翻译深度研究API 文档MCP 服务
关于我们
关于 Suppr公司介绍联系我们用户协议隐私条款
关注我们

Suppr 超能文献

核心技术专利:CN118964589B侵权必究
粤ICP备2023148730 号-1Suppr @ 2026

文献检索

告别复杂PubMed语法,用中文像聊天一样搜索,搜遍4000万医学文献。AI智能推荐,让科研检索更轻松。

立即免费搜索

文件翻译

保留排版,准确专业,支持PDF/Word/PPT等文件格式,支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述,25分钟生成高质量综述,智能提取关键信息,辅助科研写作。

立即免费体验

爱泼斯坦-巴尔病毒DNA的宿主细胞表型依赖性甲基化模式

Host cell phenotype-dependent methylation patterns of Epstein-Barr virus DNA.

作者信息

Minarovits J, Minarovits-Kormuta S, Ehlin-Henriksson B, Falk K, Klein G, Ernberg I

机构信息

Department of Tumor Biology, Karolinska Institute, Stockholm, Sweden.

出版信息

J Gen Virol. 1991 Jul;72 ( Pt 7):1591-9. doi: 10.1099/0022-1317-72-7-1591.

DOI:10.1099/0022-1317-72-7-1591
PMID:1649897
Abstract

We have shown previously that the EBNA 1 and latent membrane protein encoding regions of the Epstein-Barr virus (EBV) genome are highly methylated at CCGG sequences in the Burkitt's lymphoma (BL)-derived cell line Rael, but are unmethylated in a lymphoblastoid cell line (LCL) harbouring the same virus. To examine whether this is a regular phenomenon, we compared the methylation patterns of selected regions (BamHI C, W, H, M, E, K and N fragments) of EBV DNA in representative EBV-carrying cell types of normal and neoplastic origin. Analysis of HpaII and MspI cleavage patterns showed that all probed regions were highly methylated in all six BL biopsy samples, but hypomethylated in the four LCLs immortalized by the virus. EBV DNA was also highly methylated in the nude mouse-passaged C15 nasopharyngeal carcinoma strain and partially methylated in the C18 strain. Eight BL lines propagated in vitro, ranging from a typical BL group I to a more LCL-like group III phenotype, showed heterogeneous levels of methylation. Rael, the only stable group I cell line, carried highly methylated viral genomes. The other cell lines, which have drifted to an LCL-like blastic phenotype to various degrees, showed more moderate or low viral DNA methylation. Two sublines of the BL cell line Jijoye, which could be classified as groups II and III, respectively, showed a corresponding difference in EBV DNA methylation.(ABSTRACT TRUNCATED AT 250 WORDS)

摘要

我们之前已经表明,在源自伯基特淋巴瘤(BL)的细胞系Rael中,爱泼斯坦 - 巴尔病毒(EBV)基因组的EBNA 1和潜伏膜蛋白编码区域在CCGG序列处高度甲基化,但在携带相同病毒的淋巴母细胞系(LCL)中未甲基化。为了研究这是否是一种普遍现象,我们比较了正常和肿瘤来源的代表性携带EBV细胞类型中EBV DNA选定区域(BamHI C、W、H、M、E、K和N片段)的甲基化模式。对HpaII和MspI切割模式的分析表明,在所有六个BL活检样本中,所有检测区域都高度甲基化,但在由该病毒永生化的四个LCL中甲基化程度较低。EBV DNA在裸鼠传代的C15鼻咽癌菌株中也高度甲基化,在C18菌株中部分甲基化。八个在体外培养的BL细胞系,从典型的BL I组到更类似LCL的III组表型,显示出不同程度的甲基化。Rael是唯一稳定的I组细胞系,携带高度甲基化的病毒基因组。其他细胞系已不同程度地转变为类似LCL的母细胞表型,显示出更中等或低水平的病毒DNA甲基化。BL细胞系Jijoye的两个亚系,分别可归类为II组和III组,在EBV DNA甲基化方面表现出相应差异。(摘要截短于250字)

相似文献

1
Host cell phenotype-dependent methylation patterns of Epstein-Barr virus DNA.爱泼斯坦-巴尔病毒DNA的宿主细胞表型依赖性甲基化模式
J Gen Virol. 1991 Jul;72 ( Pt 7):1591-9. doi: 10.1099/0022-1317-72-7-1591.
2
The role of methylation in the phenotype-dependent modulation of Epstein-Barr nuclear antigen 2 and latent membrane protein genes in cells latently infected with Epstein-Barr virus.甲基化在爱泼斯坦-巴尔病毒潜伏感染细胞中对爱泼斯坦-巴尔核抗原2和潜伏膜蛋白基因的表型依赖性调控中的作用。
J Gen Virol. 1989 Nov;70 ( Pt 11):2989-3002. doi: 10.1099/0022-1317-70-11-2989.
3
Variable expression of latent membrane protein in nasopharyngeal carcinoma can be related to methylation status of the Epstein-Barr virus BNLF-1 5'-flanking region.鼻咽癌中潜伏膜蛋白的可变表达可能与爱泼斯坦-巴尔病毒BNLF-1 5'-侧翼区的甲基化状态有关。
J Virol. 1991 Mar;65(3):1558-67. doi: 10.1128/JVI.65.3.1558-1567.1991.
4
Methylation status of the Epstein-Barr virus (EBV) BamHI W latent cycle promoter and promoter activity: analysis with novel EBV-positive Burkitt and lymphoblastoid cell lines.爱泼斯坦-巴尔病毒(EBV)BamHI W潜伏周期启动子的甲基化状态及启动子活性:新型EBV阳性伯基特细胞系和淋巴母细胞系的分析
J Virol. 2006 Nov;80(21):10700-11. doi: 10.1128/JVI.01204-06. Epub 2006 Aug 18.
5
Methylation of discrete sites within the enhancer region regulates the activity of the Epstein-Barr virus BamHI W promoter in Burkitt lymphoma lines.增强子区域内离散位点的甲基化调控伯基特淋巴瘤细胞系中爱泼斯坦-巴尔病毒BamHI W启动子的活性。
J Virol. 1992 Jan;66(1):62-9. doi: 10.1128/JVI.66.1.62-69.1992.
6
An origin of DNA replication (oriP) in highly methylated episomal Epstein-Barr virus DNA localizes to a 4.5-kb unmethylated region.高度甲基化的游离型爱泼斯坦-巴尔病毒DNA中的DNA复制起点(oriP)定位于一个4.5千碱基的未甲基化区域。
Virology. 1993 Aug;195(2):608-15. doi: 10.1006/viro.1993.1412.
7
Down-regulation of integrated Epstein-Barr virus nuclear antigen 1 and 2 genes in a Burkitt lymphoma cell line after somatic cell fusion with autologous EBV-immortalized lymphoblastoid cells.与自体EB病毒永生化淋巴母细胞进行体细胞融合后,伯基特淋巴瘤细胞系中整合的爱泼斯坦-巴尔病毒核抗原1和2基因的下调。
Int J Cancer. 1993 Feb 20;53(4):621-7. doi: 10.1002/ijc.2910530416.
8
Different Epstein-Barr virus-B cell interactions in phenotypically distinct clones of a Burkitt's lymphoma cell line.伯基特淋巴瘤细胞系表型不同的克隆中不同的爱泼斯坦-巴尔病毒与B细胞的相互作用。
J Gen Virol. 1990 Jul;71 ( Pt 7):1481-95. doi: 10.1099/0022-1317-71-7-1481.
9
Integration of a short Epstein-Barr virus DNA fragment in a B95-8 virus converted Burkitt lymphoma line expressing Epstein-Barr nuclear antigens EBNA2 and EBNA5.一个短的爱泼斯坦-巴尔病毒DNA片段整合到一个表达爱泼斯坦-巴尔核抗原EBNA2和EBNA5的B95-8病毒转化的伯基特淋巴瘤细胞系中。
J Gen Virol. 1993 Jul;74 ( Pt 7):1393-8. doi: 10.1099/0022-1317-74-7-1393.
10
5-Azacytidine up regulates the expression of Epstein-Barr virus nuclear antigen 2 (EBNA-2) through EBNA-6 and latent membrane protein in the Burkitt's lymphoma line rael.5-氮杂胞苷通过EBNA-6和潜伏膜蛋白上调伯基特淋巴瘤细胞系rael中爱泼斯坦-巴尔病毒核抗原2(EBNA-2)的表达。
J Virol. 1989 Jul;63(7):3135-41. doi: 10.1128/JVI.63.7.3135-3141.1989.

引用本文的文献

1
Epstein-Barr virus-host cell interactions: an epigenetic dialog?爱泼斯坦-巴尔病毒与宿主细胞的相互作用:一种表观遗传对话?
Front Genet. 2014 Oct 21;5:367. doi: 10.3389/fgene.2014.00367. eCollection 2014.
2
Epstein-Barr virus transcription activator R upregulates BARF1 expression by direct binding to its promoter, independent of methylation.EB 病毒转录激活因子 R 通过直接结合其启动子而上调 BARF1 的表达,而与甲基化无关。
J Virol. 2012 Oct;86(20):11322-32. doi: 10.1128/JVI.01161-12. Epub 2012 Aug 15.
3
The role of promoter methylation in Epstein-Barr virus (EBV) microRNA expression in EBV-infected B cell lines.
启动子甲基化在 Epstein-Barr 病毒 (EBV) 微 RNA 表达中的作用在 EBV 感染的 B 细胞系中。
Exp Mol Med. 2011 Jul 30;43(7):401-10. doi: 10.3858/emm.2011.43.7.044.
4
Epstein-Barr virus LF2 protein regulates viral replication by altering Rta subcellular localization.EBV LF2 蛋白通过改变 Rta 的亚细胞定位来调节病毒复制。
J Virol. 2010 Oct;84(19):9920-31. doi: 10.1128/JVI.00573-10. Epub 2010 Jul 14.
5
Methylation-dependent binding of the epstein-barr virus BZLF1 protein to viral promoters.爱泼斯坦-巴尔病毒BZLF1蛋白与病毒启动子的甲基化依赖性结合。
PLoS Pathog. 2009 Mar;5(3):e1000356. doi: 10.1371/journal.ppat.1000356. Epub 2009 Mar 27.
6
High-resolution analysis of CpG methylation and in vivo protein-DNA interactions at the alternative Epstein-Barr virus latency promoters Qp and Cp in the nasopharyngeal carcinoma cell line C666-1.对鼻咽癌细胞系C666-1中爱泼斯坦-巴尔病毒潜伏性启动子Qp和Cp处的CpG甲基化及体内蛋白质-DNA相互作用进行高分辨率分析。
Virus Genes. 2007 Oct;35(2):195-202. doi: 10.1007/s11262-007-0095-y. Epub 2007 May 18.
7
Methylation status of the Epstein-Barr virus (EBV) BamHI W latent cycle promoter and promoter activity: analysis with novel EBV-positive Burkitt and lymphoblastoid cell lines.爱泼斯坦-巴尔病毒(EBV)BamHI W潜伏周期启动子的甲基化状态及启动子活性:新型EBV阳性伯基特细胞系和淋巴母细胞系的分析
J Virol. 2006 Nov;80(21):10700-11. doi: 10.1128/JVI.01204-06. Epub 2006 Aug 18.
8
BZLF1 activation of the methylated form of the BRLF1 immediate-early promoter is regulated by BZLF1 residue 186.BZLF1对BRLF1即刻早期启动子甲基化形式的激活受BZLF1第186位残基调控。
J Virol. 2005 Jun;79(12):7338-48. doi: 10.1128/JVI.79.12.7338-7348.2005.
9
Protein-DNA binding and CpG methylation at nucleotide resolution of latency-associated promoters Qp, Cp, and LMP1p of Epstein-Barr virus.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
J Virol. 2001 Mar;75(6):2584-96. doi: 10.1128/JVI.75.6.2584-2596.2001.
10
Methylation of transcription factor binding sites in the Epstein-Barr virus latent cycle promoter Wp coincides with promoter down-regulation during virus-induced B-cell transformation.在病毒诱导的B细胞转化过程中,爱泼斯坦-巴尔病毒潜伏周期启动子Wp中转录因子结合位点的甲基化与启动子下调同时发生。
J Virol. 2000 Nov;74(22):10468-79. doi: 10.1128/jvi.74.22.10468-10479.2000.