ArticleNucleic acids research2014
Epstein-Barr virus nuclear antigen 3A protein regulates CDKN2B transcription via interaction with MIZ-1.
Article in Nucleic acids research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 29 citations in OpenAlex.
- Extrachromosomal circular DNA and their roles in cancer progression.Genes & diseases · 2025Review
- HIV-associated cancers and lymphoproliferative disorders caused by Kaposi sarcoma herpesvirus and Epstein-Barr virus.Clinical microbiology reviews · 2024Review
- Review
- A DNA tumor virus globally reprograms host 3D genome architecture to achieve immortal growth.Nature communications · 2023Article
- Genotype characterization of Epstein-Barr virus among adults living with human immunodeficiency virus in Ethiopia.Frontiers in microbiology · 2023Article
- Modulation of alternative splicing during early infection of human primary B lymphocytes with Epstein-Barr virus (EBV): a novel function for the viral EBNA-LP protein.Nucleic acids research · 2021Article
- Article
- An EBNA3A-Mutated Epstein-Barr Virus Retains the Capacity for Lymphomagenesis in a Cord Blood-Humanized Mouse Model.Journal of virology · 2020Article
- The interplay between Epstein-Bar virus (EBV) with the p53 and its homologs during EBV associated malignancies.Heliyon · 2019Review
- Molecular mechanisms of EBV-driven cell cycle progression and oncogenesis.Medical microbiology and immunology · 2019Review
- Viral-Targeted Strategies Against EBV-Associated Lymphoproliferative Diseases.Frontiers in oncology · 2019Review
- Epstein-Barr Virus Nuclear Antigen 3C Inhibits Expression ofJournal of virology · 2018Article
- Epstein-Barr Virus (EBV) Latent Protein EBNA3A Directly Targets and Silences theJournal of virology · 2018Article
- The Cooperative Functions of the EBNA3 Proteins Are Central to EBV Persistence and Latency.Pathogens (Basel, Switzerland) · 2018Review
- The Epstein-Barr Virus Regulome in Lymphoblastoid Cells.Cell host & microbe · 2017Article
- EBV epigenetically suppresses the B cell-to-plasma cell differentiation pathway while establishing long-term latency.PLoS biology · 2017Article
- Epigenetic Impact on EBV Associated B-Cell Lymphomagenesis.Biomolecules · 2016Review
- Role of EBNA-3 Family Proteins in EBV Associated B-cell Lymphomagenesis.Frontiers in microbiology · 2016Review
- Epstein-Barr Virus Proteins EBNA3A and EBNA3C Together Induce Expression of the Oncogenic MicroRNA Cluster miR-221/miR-222 and Ablate Expression of Its Target p57KIP2.PLoS pathogens · 2015Article
- Epstein-Barr virus latent genes.Experimental & molecular medicine · 2015Review
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Authors and funding
12 authors at 7 institutions in 2 countries.
Funding
Abstract
The Epstein-Barr virus (EBV) nuclear antigen 3 family of protein is critical for the EBV-induced primary B-cell growth transformation process. Using a yeast two-hybrid screen we identified 22 novel cellular partners of the EBNA3s. Most importantly, among the newly identified partners, five are known to play direct and important roles in transcriptional regulation. Of these, the Myc-interacting zinc finger protein-1 (MIZ-1) is a transcription factor initially characterized as a binding partner of MYC. MIZ-1 activates the transcription of a number of target genes including the cell cycle inhibitor CDKN2B. Focusing on the EBNA3A/MIZ-1 interaction we demonstrate that binding occurs in EBV-infected cells expressing both proteins at endogenous physiological levels and that in the presence of EBNA3A, a significant fraction of MIZ-1 translocates from the cytoplasm to the nucleus. Moreover, we show that a trimeric complex composed of a MIZ-1 recognition DNA element, MIZ-1 and EBNA3A can be formed, and that interaction of MIZ-1 with nucleophosmin (NPM), one of its coactivator, is prevented by EBNA3A. Finally, we show that, in the presence of EBNA3A, expression of the MIZ-1 target gene, CDKN2B, is downregulated and repressive H3K27 marks are established on its promoter region suggesting that EBNA3A directly counteracts the growth inhibitory action of MIZ-1.
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