ArticleJournal of virology2009
Functional interaction between Epstein-Barr virus replication protein Zta and host DNA damage response protein 53BP1.
Article in Journal of virology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 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
31 citing papers in PubMed, 43 citations in OpenAlex.
- Reconstructing EBV reactivation and DNA damage response kinetics in morphologic pseudotime.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Reconstructing EBV reactivation and DNA damage response kinetics in morphologic pseudotime.bioRxiv : the preprint server for biology · 2025Article
- Seneca Valley virus infection exploits DNA damage response to facilitate viral replication.Journal of virology · 2025Article
- Immune Modulation by Epstein-Barr Virus Lytic Cycle: Relevance and Implication in Oncogenesis.Pathogens (Basel, Switzerland) · 2024Review
- Epstein-Barr virus reactivation induces divergent abortive, reprogrammed, and host shutoff states by lytic progression.PLoS pathogens · 2024Article
- Epstein-Barr virus reactivation induces divergent abortive, reprogrammed, and host shutoff states by lytic progression.bioRxiv : the preprint server for biology · 2024Article
- Article
- MC180295 Inhibited Epstein-Barr Virus-Associated Gastric Carcinoma Cell Growth by Suppressing DNA Repair and the Cell Cycle.International journal of molecular sciences · 2022Article
- Epstein-Barr virus protein BKRF4 restricts nucleosome assembly to suppress host antiviral responses.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- Structural basis of DNA methylation-dependent site selectivity of the Epstein-Barr virus lytic switch protein ZEBRA/Zta/BZLF1.Nucleic acids research · 2022Article
- The bZIP Proteins of Oncogenic Viruses.Viruses · 2020Review
- Oncogenic Properties of the EBV ZEBRA Protein.Cancers · 2020Review
- Identifying the Cellular Interactome of Epstein-Barr Virus Lytic Regulator Zta Reveals Cellular Targets Contributing to Viral Replication.Journal of virology · 2020Article
- Mechanism of activation of the BNLF2a immune evasion gene of Epstein-Barr virus by Zta.The Journal of general virology · 2018Article
- Epstein-Barr Virus Hijacks DNA Damage Response Transducers to Orchestrate Its Life Cycle.Viruses · 2017Review
- Repression of CIITA by the Epstein-Barr virus transcription factor Zta is independent of its dimerization and DNA binding.The Journal of general virology · 2016Article
- Epstein-Barr virus BZLF1 protein impairs accumulation of host DNA damage proteins at damage sites in response to DNA damage.Laboratory investigation; a journal of technical methods and pathology · 2015Article
- Article
- Review
- Selective recruitment of host factors by HSV-1 replication centers.Dong wu xue yan jiu = Zoological research · 2015Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Epstein-Barr virus (EBV; human herpesvirus 4) poses major clinical problems worldwide. Following primary infection, EBV enters a form of long-lived latency in B lymphocytes, expressing few viral genes, and it persists for the lifetime of the host with sporadic bursts of viral replication. The switch between latency and replication is governed by the action of a multifunctional viral protein Zta (also called BZLF1, ZEBRA, and Z). Using a global proteomic approach, we identified a host DNA damage repair protein that specifically interacts with Zta: 53BP1. 53BP1 is intimately connected with the ATM signal transduction pathway, which is activated during EBV replication. The interaction of 53BP1 with Zta requires the C-terminal ends of both proteins. A series of Zta mutants that show a wild-type ability to perform basic functions of Zta, such as dimer formation, interaction with DNA, and the transactivation of viral genes, were shown to have lost the ability to induce the viral lytic cycle. Each of these mutants also is compromised in the C-terminal region for interaction with 53BP1. In addition, the knockdown of 53BP1 expression reduced viral replication, suggesting that the association between Zta and 53BP1 is involved in the viral replication cycle.
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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.