ArticleEMBO reports2021
PLK1-dependent phosphorylation restrains EBNA2 activity and lymphomagenesis in EBV-infected mice.
Article in EMBO reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 9 citations in OpenAlex.
- Crystal Structures of Plk1 Polo-Box Domain Bound to the Human Papillomavirus Minor Capsid Protein L2-Derived Peptide.Journal of microbiology (Seoul, Korea) · 2023Article
- Onvansertib inhibits the proliferation and improves the cisplatin-resistance of lung adenocarcinoma via β-catenin/c-Myc signaling pathway.American journal of cancer research · 2023Article
- EBNA2 mediates lipid metabolism and tumorigenesis through activation of ATF4 pathway.American journal of cancer research · 2023Article
- Functional diversity: update of the posttranslational modification of Epstein-Barr virus coding proteins.Cellular and molecular life sciences : CMLS · 2022Review
- Do Epstein-Barr Virus Mutations and Natural Genome Sequence Variations Contribute to Disease?Biomolecules · 2021Review
- PLK1-dependent phosphorylation restrains EBNA2 activity and lymphomagenesis in EBV-infected mice.EMBO reports · 2021Article
Corrections and comments
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Authors and funding
17 authors at 5 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
While Epstein-Barr virus (EBV) establishes a life-long latent infection in apparently healthy human immunocompetent hosts, immunodeficient individuals are at particular risk to develop lymphoproliferative B-cell malignancies caused by EBV. A key EBV protein is the transcription factor EBV nuclear antigen 2 (EBNA2), which initiates B-cell proliferation. Here, we combine biochemical, cellular, and in vivo experiments demonstrating that the mitotic polo-like kinase 1 (PLK1) binds to EBNA2, phosphorylates its transactivation domain, and thereby inhibits its biological activity. EBNA2 mutants that impair PLK1 binding or prevent EBNA2 phosphorylation are gain-of-function mutants. They exhibit enhanced transactivation capacities, accelerate the proliferation of infected B cells, and promote the development of monoclonal B-cell lymphomas in infected mice. Thus, PLK1 coordinates the activity of EBNA2 to attenuate the risk of tumor incidences in favor of the establishment of latency in the infected but healthy host.
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