ArticlePLoS pathogens2010
Epigenetic repression of p16(INK4A) by latent Epstein-Barr virus requires the interaction of EBNA3A and EBNA3C with CtBP.
Article in PLoS pathogens, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 102 papers.
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Who cites it
102 citing papers in PubMed, 138 citations in OpenAlex.
- Modulation of DNA Damage by Epstein-Barr Virus (EBV).Viruses · 2026Review
- Epstein-Barr virus (EBV) infection causes human germinal center B cell-derived lymphomas in the absence of EBNA2 expression.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Epigenetic activation of EBV BGLF4 determines antiviral-based regimen response in EBV+CNS lymphoproliferative disease.Blood neoplasia · 2026Article
- CRISPR Screens Reveal Epstein-Barr Virus-activated JunB as a Key Lymphoblastoid B cell Dependency Factor that Represses Cyclin Dependent Kinase Inhibitor P18INK4c.bioRxiv : the preprint server for biology · 2026Article
- Multiple sclerosis and infection: history, EBV, and the search for mechanism.Microbiology and molecular biology reviews : MMBR · 2025Review
- A thorough insight into the life cycle of the Epstein-Barr virus. From the molecular to the organismal level.Current research in microbial sciences · 2025Review
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- Epstein-Barr virus and host cell 3D genome organization.Journal of medical virology · 2023Review
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- A DNA tumor virus globally reprograms host 3D genome architecture to achieve immortal growth.Nature communications · 2023Article
- LMP1 and EBNA2 constitute a minimal set of EBV genes for transformation of human B cells.Frontiers in immunology · 2023Article
- AhR Promotes the Development of Non-small cell lung cancer by Inducing SLC7A11-dependent Antioxidant Function.Journal of Cancer · 2023Article
- Regulation of B cell receptor signalling by Epstein-Barr virus nuclear antigens.The Biochemical journal · 2022Article
- Cancers associated with human gammaherpesviruses.The FEBS journal · 2022Review
- Time-resolved transcriptomes reveal diverse B cell fate trajectories in the early response to Epstein-Barr virus infection.Cell reports · 2022Article
- Epstein-Barr virus infection is associated with the nuclear factor-kappa B p65 signaling pathway in renal cell carcinoma.BMC urology · 2022Article
- Epstein-Barr virus perpetuates B cell germinal center dynamics and generation of autoimmune-associated phenotypesFrontiers in immunology · 2022Article
- Oncogenic Viruses as Entropic Drivers of Cancer Evolution.Frontiers in virology (Lausanne, Switzerland) · 2021Article
- The Epstein-Barr virus noncoding RNA EBER2 transactivates the UCHL1 deubiquitinase to accelerate cell growth.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
42 more citing papers are in PubMed but not listed here.
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
As an inhibitor of cyclin-dependent kinases, p16(INK4A) is an important tumour suppressor and inducer of cellular senescence that is often inactivated during the development of cancer by promoter DNA methylation. Using newly established lymphoblastoid cell lines (LCLs) expressing a conditional EBNA3C from recombinant EBV, we demonstrate that EBNA3C inactivation initiates chromatin remodelling that resets the epigenetic status of p16(INK4A) to permit transcriptional activation: the polycomb-associated repressive H3K27me3 histone modification is substantially reduced, while the activation-related mark H3K4me3 is modestly increased. Activation of EBNA3C reverses the distribution of these epigenetic marks, represses p16(INK4A) transcription and allows proliferation. LCLs lacking EBNA3A express relatively high levels of p16(INK4A) and have a similar pattern of histone modifications on p16(INK4A) as produced by the inactivation of EBNA3C. Since binding to the co-repressor of transcription CtBP has been linked to the oncogenic activity of EBNA3A and EBNA3C, we established LCLs with recombinant viruses encoding EBNA3A- and/or EBNA3C-mutants that no longer bind CtBP. These novel LCLs have revealed that the chromatin remodelling and epigenetic repression of p16(INK4A) requires the interaction of both EBNA3A and EBNA3C with CtBP. The repression of p16(INK4A) by latent EBV will not only overcome senescence in infected B cells, but may also pave the way for p16(INK4A) DNA methylation during B cell lymphomagenesis.
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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.