ArticlePLoS pathogens2011
Epstein-Barr virus nuclear antigen 3C stabilizes Gemin3 to block p53-mediated apoptosis.
Article in PLoS pathogens, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 47 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
47 citing papers in PubMed, 65 citations in OpenAlex.
- IRF-4-mediated CIITA transcription is blocked by KSHV encoded LANA to inhibit MHC II presentation.PLoS pathogens · 2013Trial
- African swine fever virus MGF360-9L degrades DDX20 through the Rab1A-dependent autophagy pathway to antagonize its antiviral effect.Virologica Sinica · 2025Article
- DDX20: A Multifunctional Complex Protein.Molecules (Basel, Switzerland) · 2023Review
- Cancers associated with human gammaherpesviruses.The FEBS journal · 2022Review
- Metabolic Control by DNA Tumor Virus-Encoded Proteins.Pathogens (Basel, Switzerland) · 2021Review
- Retraction: Epstein-Barr Virus Nuclear Antigen 3C Stabilizes Gemin3 to Block p53-mediated Apoptosis.PLoS pathogens · 2021Article
- The Mitochondrial Protein VDAC1 at the Crossroads of Cancer Cell Metabolism: The Epigenetic Link.Cancers · 2020Article
- Proteasomal inhibition triggers viral oncoprotein degradation via autophagy-lysosomal pathway.PLoS pathogens · 2020Article
- A subset of SMN complex members have a specific role in tissue regeneration via ERBB pathway-mediated proliferation.NPJ Regenerative medicine · 2020Article
- Polyploid Giant Cancer Cells, a Hallmark of Oncoviruses and a New Therapeutic Challenge.Frontiers in oncology · 2020Review
- Analysis of the expression, function, prognosis and co-expression genes of DDX20 in gastric cancer.Computational and structural biotechnology journal · 2020Article
- The interplay between Epstein-Bar virus (EBV) with the p53 and its homologs during EBV associated malignancies.Heliyon · 2019Review
- The scope of viral causation of human cancers: interpreting virus density from an evolutionary perspective.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2019Article
- EBNA3C facilitates RASSF1A downregulation through ubiquitin-mediated degradation and promoter hypermethylation to drive B-cell proliferation.PLoS pathogens · 2019Article
- Viral-Targeted Strategies Against EBV-Associated Lymphoproliferative Diseases.Frontiers in oncology · 2019Review
- Epstein-Barr Virus MicroRNA miR-BART5-3p Inhibits p53 Expression.Journal of virology · 2018Article
- Review
- Operation of mitochondrial machinery in viral infection-induced immune responses.Biochemical pharmacology · 2018Review
- Human Oncoviruses and p53 Tumor Suppressor Pathway Deregulation at the Origin of Human Cancers.Cancers · 2018Review
- Transcriptional and epigenetic modulation of autophagy promotes EBV oncoprotein EBNA3C induced B-cell survival.Cell death & disease · 2018Article
Corrections and comments
- Retraction · 2021-04-30Concerns/Issues about Data · Duplication of/in Image · Error in Image · Manipulation of Images · Original Data and/or Images not Provided and/or not Available · · see also: https://pubpeer.com/publications/DFA7DEFF22AB14DCB3DA72141D77ED#4
- Retracted
Authors and funding
8 authors at 2 institutions in 2 countries.
Funding
Abstract
The Epstein-Barr nuclear antigen 3C (EBNA3C), one of the essential latent antigens for Epstein-Barr virus (EBV)-induced immortalization of primary human B lymphocytes in vitro, has been implicated in regulating cell proliferation and anti-apoptosis via interaction with several cellular and viral factors. Gemin3 (also named DDX20 or DP103) is a member of DEAD RNA helicase family which exhibits diverse cellular functions including DNA transcription, recombination and repair, and RNA metabolism. Gemin3 was initially identified as a binding partner to EBNA2 and EBNA3C. However, the mechanism by which EBNA3C regulates Gemin3 function remains unclear. Here, we report that EBNA3C directly interacts with Gemin3 through its C-terminal domains. This interaction results in increased stability of Gemin3 and its accumulation in both B lymphoma cells and EBV transformed lymphoblastoid cell lines (LCLs). Moreover, EBNA3C promotes formation of a complex with p53 and Gemin3 which blocks the DNA-binding affinity of p53. Small hairpin RNA based knockdown of Gemin3 in B lymphoma or LCL cells remarkably attenuates the ability of EBNA3C to inhibit the transcription activity of p53 on its downstream genes p21 and Bax, as well as apoptosis. These findings provide the first evidence that Gemin3 may be a common target of oncogenic viruses for driving cell proliferation and anti-apoptotic activities.
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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.