ArticleOncotarget2015
EBNA3C regulates p53 through induction of Aurora kinase B.
Article in Oncotarget, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
What it found
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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.
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Who cites it
20 citing papers in PubMed, 30 citations in OpenAlex.
- Interplay of aurora kinase a functional residues and Epstein-barr Nuclear Antigen 1 in Epstein-barr virus associated Gastric cancer using AGS cells.BMC cancer · 2025Article
- Cancers associated with human gammaherpesviruses.The FEBS journal · 2022Review
- Kinases and therapeutics in pathogen mediated gastric cancer.Molecular biology reports · 2022Review
- Article
- Aurora Kinase B Inhibition: A Potential Therapeutic Strategy for Cancer.Molecules (Basel, Switzerland) · 2021Review
- Viral strategies for circumventing p53: the case of severe acute respiratory syndrome coronavirus.Current opinion in oncology · 2021Review
- Mitotic and DNA Damage Response Proteins: Maintaining the Genome Stability and Working for the Common Good.Frontiers in cell and developmental biology · 2021Review
- RNA Sequencing Analyses of Gene Expression during Epstein-Barr Virus Infection of Primary B Lymphocytes.Journal of virology · 2019Article
- Frequency of Epstein–Barr Virus DNA in Formalin-Fixed Paraffin-Embedded Tissue of Patients with Ductal Breast CarcinomaAsian Pacific journal of cancer prevention : APJCP · 2019Article
- EBNA3C facilitates RASSF1A downregulation through ubiquitin-mediated degradation and promoter hypermethylation to drive B-cell proliferation.PLoS pathogens · 2019Article
- Epstein-Barr Virus MicroRNA miR-BART5-3p Inhibits p53 Expression.Journal of virology · 2018Article
- An EBNA3C-deleted Epstein-Barr virus (EBV) mutant causes B-cell lymphomas with delayed onset in a cord blood-humanized mouse model.PLoS pathogens · 2018Article
- Transcriptional and epigenetic modulation of autophagy promotes EBV oncoprotein EBNA3C induced B-cell survival.Cell death & disease · 2018Article
- Review
- A post-translational modification switch controls coactivator function of histone methyltransferases G9a and GLP.EMBO reports · 2017Article
- KSHV-Mediated Regulation of Par3 and SNAIL Contributes to B-Cell Proliferation.PLoS pathogens · 2016Article
- Inhibiting cell migration and cell invasion by silencing the transcription factor ETS-1 in human bladder cancer.Oncotarget · 2016Article
- The Role of Gammaherpesviruses in Cancer Pathogenesis.Pathogens (Basel, Switzerland) · 2016Review
- Epstein-Barr Virus: Diseases Linked to Infection and Transformation.Frontiers in microbiology · 2016Review
- Role of EBNA-3 Family Proteins in EBV Associated B-cell Lymphomagenesis.Frontiers in microbiology · 2016Review
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
In multicellular organisms p53 maintains genomic integrity through activation of DNA repair, and apoptosis. EBNA3C can down regulate p53 transcriptional activity. Aurora kinase (AK) B phosphorylates p53, which leads to degradation of p53. Aberrant expression of AK-B is a hallmark of numerous human cancers. Therefore changes in the activities of p53 due to AK-B and EBNA3C expression is important for understanding EBV-mediated cell transformation. Here we show that the activities of p53 and its homolog p73 are dysregulated in EBV infected primary cells which can contribute to increased cell transformation. Further, we showed that the ETS-1 binding site is crucial for EBNA3C-mediated up-regulation of AK-B transcription. Further, we determined the Ser 215 residue of p53 is critical for functional regulation by AK-B and EBNA3C and that the kinase domain of AK-B which includes amino acid residues 106, 111 and 205 was important for p53 regulation. AK-B with a mutation at residue 207 was functionally similar to wild type AK-B in terms of its kinase activities and knockdown of AK-B led to enhanced p73 expression independent of p53. This study explores an additional mechanism by which p53 is regulated by AK-B and EBNA3C contributing to EBV-induced B-cell transformation.
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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.