ArticleJournal of virology2002
Separation of the DNA replication, segregation, and transcriptional activation functions of Epstein-Barr nuclear antigen 1.
Article in Journal of virology, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 66 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
66 citing papers in PubMed, 119 citations in OpenAlex.
- EBNA1 inhibitors reveal CDC7 and POU2F1 as direct functional targets in EBV epithelial cancers.mBio · 2026Article
- EBV Latency Programs: Molecular and Epigenetic Regulation and Its Role in Disease Pathogenesis.Journal of medical virology · 2025Review
- Epstein-Barr virus-infected nasopharyngeal carcinoma therapeutics: oncoprotein targets and clinical implications.Medical oncology (Northwood, London, England) · 2025Review
- Sequence variation of the Epstein-Barr virus nuclear antigen 1 (EBNA1) gene in chronic lymphocytic leukemia and healthy volunteer subjects.Archives of virology · 2023Article
- Cancers associated with human gammaherpesviruses.The FEBS journal · 2022Review
- The Epstein-Barr Virus Enhancer Interaction Landscapes in Virus-Associated Cancer Cell Lines.Journal of virology · 2022Article
- EBV-associated diseases: Current therapeutics and emerging technologies.Frontiers in immunology · 2022Review
- Antibodies from Multiple Sclerosis Brain Identified Epstein-Barr Virus Nuclear Antigen 1 & 2 Epitopes which Are Recognized by Oligoclonal Bands.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2021Article
- 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
- Review
- Analysis of Epstein-Barr Virus Genomes and Expression Profiles in Gastric Adenocarcinoma.Journal of virology · 2018Article
- EBNA1-targeted inhibitors: Novel approaches for the treatment of Epstein-Barr virus-associated cancers.Theranostics · 2018Review
- IFNγ induces PD-L1 overexpression by JAK2/STAT1/IRF-1 signaling in EBV-positive gastric carcinoma.Scientific reports · 2017Article
- Article
- The value of circulating CYFRA21-1 expression in patients with nasopharyngeal carcinoma: a study of 529 subjects.International journal of clinical oncology · 2016Article
- ERK2 phosphorylation of EBNA1 serine 383 residue is important for EBNA1-dependent transactivation.Oncotarget · 2016Article
- Article
- Epstein-Barr virus latent genes.Experimental & molecular medicine · 2015Review
- Article
6 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In latent Epstein-Barr virus infection, the viral EBNA1 protein binds to specific sites in the viral origin of DNA replication, oriP, to activate the initiation of DNA replication, enhance the expression of other viral latency proteins, and partition the viral episomes during cell division. The DNA binding domain of EBNA1 is required for all three function, and a Gly-Arg-rich sequence between amino acids 325 and 376 is required for both the transcriptional activation and partitioning functions. We have used mutational analysis to identify additional EBNA1 sequences that contribute to EBNA1 functions. We show that EBNA1 amino acids 8 to 67 contribute to, but are not absolutely required for, EBNA1 replication, partitioning, and transcriptional activation functions. A Gly-Arg-rich sequence (amino acids 33 to 53) that is similar to that of amino acids 325 to 376 and lies within the 8-to-67 region was not responsible for the functional contributions of residues 8 to 67, since deletion of amino acids 34 to 52 alone did not affect EBNA1 functions. We also found that deletion of amino acids 61 to 83 eliminated the transcriptional activity of EBNA1 without affecting partitioning. This mutant also exhibited an increased replication efficiency that resulted in the maintenance of oriP plasmids at a copy number approximately fourfold higher than for wild-type EBNA1. The results indicate that the three EBNA1 functions have overlapping but different sequence requirements. Transcriptional activation requires residues 61 to 83 and 325 to 376 and is stimulated by residues 8 to 67; partitioning requires residues 325 to 376 and is stimulated by residues 8 to 67; and replication involves redundant contributions of both the 325-to-376 and 8-to-67 regions.
Indexed as
Identifiers
What OpenQuestion holds
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.