ArticlePLoS pathogens2009
Zinc coordination is required for and regulates transcription activation by Epstein-Barr nuclear antigen 1.
Article in PLoS pathogens, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 37 citations in OpenAlex.
- From infection to infertility: a review of the role of human papillomavirus-induced oxidative stress on reproductive health and infertility.European journal of medical research · 2025Review
- Epstein-Barr Virus BRRF1 Induces Butyrophilin 2A1 in Nasopharyngeal Carcinoma NPC43 Cells via the IL-22/JAK3-STAT3 Pathway.International journal of molecular sciences · 2024Article
- Epstein-Barr virus-acquired immunodeficiency in myalgic encephalomyelitis-Is it present in long COVID?Journal of translational medicine · 2023Review
- Cryo-EM Structure and Functional Studies of EBNA1 Binding to the Family of Repeats and Dyad Symmetry Elements of Epstein-Barr VirusJournal of virology · 2022Article
- Epigenetic specifications of host chromosome docking sites for latent Epstein-Barr virus.Nature communications · 2020Article
- Targeting Epstein-Barr Virus in Nasopharyngeal Carcinoma.Frontiers in oncology · 2020Review
- Ammonia generation by tryptophan synthase drives a key genetic difference between genital and ocularProceedings of the National Academy of Sciences of the United States of America · 2019Article
- Chlamydia trachomatis-infected cells and uninfected-bystander cells exhibit diametrically opposed responses to interferon gamma.Scientific reports · 2018Article
- Review
- EBNA1-targeted inhibitors: Novel approaches for the treatment of Epstein-Barr virus-associated cancers.Theranostics · 2018Review
- Crystal structure of the UBR-box from UBR6/FBXO11 reveals domain swapping mediated by zinc binding.Protein science : a publication of the Protein Society · 2017Article
- Structural and Functional Basis for an EBNA1 Hexameric Ring in Epstein-Barr Virus Episome Maintenance.Journal of virology · 2017Article
- Cell Intrinsic Factors Modulate the Effects of IFNγ on the Development ofJournal of bacteriology & parasitology · 2016Article
- Identification of MEF2B, EBF1, and IL6R as Direct Gene Targets of Epstein-Barr Virus (EBV) Nuclear Antigen 1 Critical for EBV-Infected B-Lymphocyte Survival.Journal of virology · 2016Article
- Article
- Small molecule inhibition of Epstein-Barr virus nuclear antigen-1 DNA binding activity interferes with replication and persistence of the viral genome.Antiviral research · 2014Article
- Nucleolin is important for Epstein-Barr virus nuclear antigen 1-mediated episome binding, maintenance, and transcription.Proceedings of the National Academy of Sciences of the United States of America · 2014Article
- Keeping it quiet: chromatin control of gammaherpesvirus latency.Nature reviews. Microbiology · 2013Review
- Efficient replication of Epstein-Barr virus-derived plasmids requires tethering by EBNA1 to host chromosomes.Journal of virology · 2013Article
- Oxygen-dependent expression of cytochrome c oxidase subunit 4-2 gene expression is mediated by transcription factors RBPJ, CXXC5 and CHCHD2.Nucleic acids research · 2013Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Epstein-Barr Nuclear Antigen 1 (EBNA1) is essential for Epstein-Barr virus to immortalize naïve B-cells. Upon binding a cluster of 20 cognate binding-sites termed the family of repeats, EBNA1 transactivates promoters for EBV genes that are required for immortalization. A small domain, termed UR1, that is 25 amino-acids in length, has been identified previously as essential for EBNA1 to activate transcription. In this study, we have elucidated how UR1 contributes to EBNA1's ability to transactivate. We show that zinc is necessary for EBNA1 to activate transcription, and that UR1 coordinates zinc through a pair of essential cysteines contained within it. UR1 dimerizes upon coordinating zinc, indicating that EBNA1 contains a second dimerization interface in its amino-terminus. There is a strong correlation between UR1-mediated dimerization and EBNA1's ability to transactivate cooperatively. Point mutants of EBNA1 that disrupt zinc coordination also prevent self-association, and do not activate transcription cooperatively. Further, we demonstrate that UR1 acts as a molecular sensor that regulates the ability of EBNA1 to activate transcription in response to changes in redox and oxygen partial pressure (pO(2)). Mild oxidative stress mimicking such environmental changes decreases EBNA1-dependent transcription in a lymphoblastoid cell-line. Coincident with a reduction in EBNA1-dependent transcription, reductions are observed in EBNA2 and LMP1 protein levels. Although these changes do not affect LCL survival, treated cells accumulate in G0/G1. These findings are discussed in the context of EBV latency in body compartments that differ strikingly in their pO(2) and redox potential.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.