Suppr超能文献

Sp细胞转录因子对水痘-带状疱疹病毒(VZV)IE62蛋白激活病毒启动子的差异作用。

Differential effects of Sp cellular transcription factors on viral promoter activation by varicella-zoster virus (VZV) IE62 protein.

作者信息

Khalil Mohamed I, Ruyechan William T, Hay John, Arvin Ann

机构信息

Departments of Pediatrics and Microbiology & Immunology, Stanford University School of Medicine, Stanford, CA, United States; Department of Molecular Biology, National Research Center EL-Buhouth St., Dokki, Cairo, Egypt.

Department of Microbiology and Immunology and the Witebsky Center for Microbial Pathogenesis and Immunology, University at Buffalo, Buffalo, NY, United States.

出版信息

Virology. 2015 Nov;485:47-57. doi: 10.1016/j.virol.2015.06.031. Epub 2015 Jul 23.

Abstract

The immediate early (IE) 62 protein is the major varicella-zoster virus (VZV) regulatory factor. Analysis of the VZV genome revealed 40 predicted GC-rich boxes within 36 promoters. We examined effects of ectopic expression of Sp1-Sp4 on IE62- mediated transactivation of three viral promoters. Ectopic expression of Sp3 and Sp4 enhanced IE62 activation of ORF3 and gI promoters while Sp3 reduced IE62 activation of ORF28/29 promoter and VZV DNA replication. Sp2 reduced IE62 transactivation of gI while Sp1 had no significant influence on IE62 activation with any of these viral promoters. Electrophoretic mobility shift assays (EMSA) confirmed binding of Sp1 and Sp3 but not Sp2 and Sp4 to the gI promoter. Sp1-4 bound to IE62 and amino acids 238-258 of IE62 were important for the interaction with Sp3 and Sp4 as well as Sp1. This work shows that Sp family members have differential effects on IE62-mediated transactivation in a promoter-dependent manner.

摘要

即刻早期(IE)62蛋白是水痘-带状疱疹病毒(VZV)的主要调节因子。对VZV基因组的分析显示,在36个启动子中有40个预测的富含GC的框。我们研究了Sp1-Sp4异位表达对IE62介导的三个病毒启动子反式激活的影响。Sp3和Sp4的异位表达增强了IE62对ORF3和gI启动子的激活,而Sp3降低了IE62对ORF28/29启动子的激活以及VZV DNA复制。Sp2降低了IE62对gI的反式激活,而Sp1对这些病毒启动子中任何一个的IE62激活均无显著影响。电泳迁移率变动分析(EMSA)证实Sp1和Sp3与gI启动子结合,但Sp2和Sp4不结合。Sp1-4与IE62结合,IE62的238-258位氨基酸对于与Sp3、Sp4以及Sp1的相互作用很重要。这项工作表明,Sp家族成员以启动子依赖的方式对IE62介导的反式激活具有不同的影响。

相似文献

2
Regulation of the varicella-zoster virus ORF3 promoter by cellular and viral factors.
Virology. 2013 Jun 5;440(2):171-81. doi: 10.1016/j.virol.2013.02.019. Epub 2013 Mar 21.
3
Analysis of IE62 mutations found in Varicella-Zoster virus vaccine strains for transactivation activity.
J Microbiol. 2018 Jun;56(6):441-448. doi: 10.1007/s12275-018-8144-x. Epub 2018 Jun 1.
4
Cellular transcription factor YY1 mediates the varicella-zoster virus (VZV) IE62 transcriptional activation.
Virology. 2014 Jan 20;449:244-53. doi: 10.1016/j.virol.2013.11.029. Epub 2013 Dec 12.
5
Cellular factors and IE62 activation of VZV promoters.
J Med Virol. 2003;70 Suppl 1:S90-4. doi: 10.1002/jmv.10328.
7
Role of the IE62 consensus binding site in transactivation by the varicella-zoster virus IE62 protein.
J Virol. 2010 Apr;84(8):3767-79. doi: 10.1128/JVI.02522-09. Epub 2010 Feb 3.
8
Cellular and viral factors regulate the varicella-zoster virus gE promoter during viral replication.
J Virol. 2007 Oct;81(19):10258-67. doi: 10.1128/JVI.00553-07. Epub 2007 Jul 18.
10
Interferon Gamma Inhibits Varicella-Zoster Virus Replication in a Cell Line-Dependent Manner.
J Virol. 2019 May 29;93(12). doi: 10.1128/JVI.00257-19. Print 2019 Jun 15.

引用本文的文献

1
Sp1 facilitates continued HSV-1 gene expression in the absence of key viral transactivators.
mBio. 2024 Mar 13;15(3):e0347923. doi: 10.1128/mbio.03479-23. Epub 2024 Feb 13.
2
HPV upregulates MARCHF8 ubiquitin ligase and inhibits apoptosis by degrading the death receptors in head and neck cancer.
PLoS Pathog. 2023 Mar 3;19(3):e1011171. doi: 10.1371/journal.ppat.1011171. eCollection 2023 Mar.
3
Relationship Between G-Quadruplex Sequence Composition in Viruses and Their Hosts.
Molecules. 2019 May 20;24(10):1942. doi: 10.3390/molecules24101942.
4
Analysis of IE62 mutations found in Varicella-Zoster virus vaccine strains for transactivation activity.
J Microbiol. 2018 Jun;56(6):441-448. doi: 10.1007/s12275-018-8144-x. Epub 2018 Jun 1.

本文引用的文献

1
Cellular transcription factor YY1 mediates the varicella-zoster virus (VZV) IE62 transcriptional activation.
Virology. 2014 Jan 20;449:244-53. doi: 10.1016/j.virol.2013.11.029. Epub 2013 Dec 12.
2
Regulation of the varicella-zoster virus ORF3 promoter by cellular and viral factors.
Virology. 2013 Jun 5;440(2):171-81. doi: 10.1016/j.virol.2013.02.019. Epub 2013 Mar 21.
5
Role of the IE62 consensus binding site in transactivation by the varicella-zoster virus IE62 protein.
J Virol. 2010 Apr;84(8):3767-79. doi: 10.1128/JVI.02522-09. Epub 2010 Feb 3.
6
Regulation of the ORF61 promoter and ORF61 functions in varicella-zoster virus replication and pathogenesis.
J Virol. 2009 Aug;83(15):7560-72. doi: 10.1128/JVI.00118-09. Epub 2009 May 20.
7
Cellular transcription factors Sp1 and Sp3 suppress varicella-zoster virus origin-dependent DNA replication.
J Virol. 2008 Dec;82(23):11723-33. doi: 10.1128/JVI.01322-08. Epub 2008 Sep 24.
8
Cellular and viral factors regulate the varicella-zoster virus gE promoter during viral replication.
J Virol. 2007 Oct;81(19):10258-67. doi: 10.1128/JVI.00553-07. Epub 2007 Jul 18.
10
The varicella-zoster virus (VZV) ORF9 protein interacts with the IE62 major VZV transactivator.
J Virol. 2007 Jan;81(2):761-74. doi: 10.1128/JVI.01274-06. Epub 2006 Nov 1.

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍。

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

文档翻译

学术文献翻译模型,支持多种主流文档格式。

立即体验