ArticleThe Journal of general virology2009
The Epstein-Barr virus lytic cycle activator Zta interacts with methylated ZRE in the promoter of host target gene egr1.
Article in The Journal of general virology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
What it found
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Who cites it
26 citing papers in PubMed.
- Metagenomic analysis of blood virome in ischemic stroke reveals an increase in herpesvirus transcripts and host immune activation.Genome medicine · 2026Article
- Epstein-Barr virus immediate-early protein Zta mediates the proliferation and migration of HER2-overexpressing cancer cells.Archives of virology · 2023Article
- Epstein-Barr virus inactivates the transcriptome and disrupts the chromatin architecture of its host cell in the first phase of lytic reactivation.Nucleic acids research · 2021Article
- Epstein-Barr Virus Limits the Accumulation of IPO7, an Essential Gene Product.Frontiers in microbiology · 2021Article
- Interaction sites of the Epstein-Barr virus Zta transcription factor with the host genome in epithelial cells.Access microbiology · 2021Article
- Early Growth Response Gene Upregulation in Epstein-Barr Virus (EBV)-Associated Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS).Biomolecules · 2020Review
- MicroRNA-Related Polymorphisms in Infectious Diseases-Tiny Changes With a Huge Impact on Viral Infections and Potential Clinical Applications.Frontiers in immunology · 2018Review
- S1PR1 drives a feedforward signalling loop to regulate BATF3 and the transcriptional programme of Hodgkin lymphoma cells.Leukemia · 2018Article
- Egr-1 regulates RTA transcription through a cooperative involvement of transcriptional regulators.Oncotarget · 2017Article
- Status of Epstein-Barr Virus Coinfection withJournal of oncology · 2017Review
- The Role of Gammaherpesviruses in Cancer Pathogenesis.Pathogens (Basel, Switzerland) · 2016Review
- Epstein-Barr virus transcription factor Zta acts through distal regulatory elements to directly control cellular gene expression.Nucleic acids research · 2015Article
- Regulation of the latent-lytic switch in Epstein-Barr virus.Seminars in cancer biology · 2014Review
- Epstein-Barr virus-induced epigenetic alterations following transient infection.International journal of cancer · 2013Article
- Epigenetic control of Epstein-Barr virus transcription - relevance to viral life cycle?Frontiers in genetics · 2013Article
- 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.Journal of virology · 2012Article
- Methylation profiling of Epstein-Barr virus immediate-early gene promoters, BZLF1 and BRLF1 in tumors of epithelial, NK- and B-cell origins.BMC cancer · 2012Article
- Epigenetic mechanisms in virus-induced tumorigenesis.Clinical epigenetics · 2011Article
- Virus reactivation: a panoramic view in human infections.Future virology · 2011Article
- Epigenetic control of viral life-cycle by a DNA-methylation dependent transcription factor.PloS one · 2011Article
Corrections and comments
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Authors and funding
4 authors.
Funding
Abstract
Activation of the host gene egr1 is essential for the lytic replication of Epstein-Barr virus (EBV). egr1 is activated by Zta (BZLF1, ZEBRA). Zta interacts directly with DNA through a series of closely related Zta-response elements (ZREs). Here we dissect the mechanism used by Zta to interact with the egr1 promoter and identify a weak interaction with egr1ZRE that is dependent on the distal part of egr1ZRE. Furthermore, we demonstrate that the ability of Zta to interact with egr1ZRE is enhanced at least tenfold by methylation. The ability of Zta to transactivate a reporter construct driven by the egr1 promoter can be enhanced by methylation. As the ability of Zta to interact with a methylated ZRE in the EBV genome correlates with its ability to activate the expression of the endogenous viral gene BRLF1, this suggests that Zta may also have the capability to overturn epigenetic control of egr1.
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