ArticleProceedings of the National Academy of Sciences of the United States of America2013
Latency of Epstein-Barr virus is disrupted by gain-of-function mutant cellular AP-1 proteins that preferentially bind methylated DNA.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 20 citations in OpenAlex.
- Reactivation and Management of Endogenous Latent Herpesviruses in the Spaceflight Environment.Current microbiology · 2026Review
- Replication Compartments-The Great Survival Strategy for Epstein-Barr Virus Lytic Replication.Microorganisms · 2022Review
- Structural basis of DNA methylation-dependent site selectivity of the Epstein-Barr virus lytic switch protein ZEBRA/Zta/BZLF1.Nucleic acids research · 2022Article
- Epigenetic lifestyle of Epstein-Barr virus.Seminars in immunopathology · 2020Review
- Identification of ARKL1 as a Negative Regulator of Epstein-Barr Virus Reactivation.Journal of virology · 2019Article
- A Noncanonical Basic Motif of Epstein-Barr Virus ZEBRA Protein Facilitates Recognition of Methylated DNA, High-Affinity DNA Binding, and Lytic Activation.Journal of virology · 2019Article
- Detecting and interpreting DNA methylation marks.Current opinion in structural biology · 2018Review
- Mutant Cellular AP-1 Proteins Promote Expression of a Subset of Epstein-Barr Virus Late Genes in the Absence of Lytic Viral DNA Replication.Journal of virology · 2018Article
- Epstein-Barr Virus Rta-Mediated Accumulation of DNA Methylation Interferes with CTCF Binding in both Host and Viral Genomes.Journal of virology · 2017Article
- Methyl-dependent and spatial-specific DNA recognition by the orthologous transcription factors human AP-1 and Epstein-Barr virus Zta.Nucleic acids research · 2017Article
- ERK/c-Jun Recruits Tet1 to Induce Zta Expression and Epstein-Barr Virus Reactivation through DNA Demethylation.Scientific reports · 2016Article
- Epstein-Barr virus lytic reactivation regulation and its pathogenic role in carcinogenesis.International journal of biological sciences · 2016Review
- 5-hydroxymethylation of the EBV genome regulates the latent to lytic switch.Proceedings of the National Academy of Sciences of the United States of America · 2015Article
- Regulation of the latent-lytic switch in Epstein-Barr virus.Seminars in cancer biology · 2014Review
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 3 countries.
Funding
Abstract
ZEBReplication Activator (ZEBRA), a viral basic zipper protein that initiates the Epstein-Barr viral lytic cycle, binds to DNA and activates transcription through heptamer ZEBRA response elements (ZREs) related to AP-1 sites. A component of the biologic action of ZEBRA is attributable to binding methylated CpGs in ZREs present in the promoters of viral lytic cycle genes. Residue S186 of ZEBRA, Z(S186), which is absolutely required for disruption of latency, participates in the recognition of methylated DNA. We find that mutant cellular AP-1 proteins, Jun(A266S) and Fos(A151S), with alanine-to-serine substitutions homologous to Z(S186), exhibit altered DNA-binding affinity and preferentially bind methylated ZREs. These mutant AP-1 proteins acquire functions of ZEBRA; they activate expression of many viral early lytic cycle gene transcripts in cells harboring latent EBV but are selectively defective in activating expression of some viral proteins and are unable to promote viral DNA replication. Transcriptional activation by mutant c-Jun and c-Fos that have acquired the capacity to bind methylated CpG challenges the paradigm that DNA methylation represses gene expression.
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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.