ReviewFuture microbiology2013
Impact of EBV essential nuclear protein EBNA-3C on B-cell proliferation and apoptosis.
Review in Future microbiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
29 citing papers in PubMed.
- Review
- Review
- Molecular mechanisms of viral oncogenesis in haematological malignancies: perspectives from metabolic reprogramming, epigenetic regulation and immune microenvironment remodeling.Experimental hematology & oncology · 2025Review
- Anti-Epstein-Barr Virus Activities of Flavones and Flavonols with Effects on Virus-Related Cancers.Molecules (Basel, Switzerland) · 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
- The role of viruses in HIV-associated lymphomas.Seminars in hematology · 2022Article
- Virus-Mediated Inhibition of Apoptosis in the Context of EBV-Associated Diseases: Molecular Mechanisms and Therapeutic Perspectives.International journal of molecular sciences · 2022Review
- Unraveling the links between neurodegeneration and Epstein-Barr virus-mediated cell cycle dysregulation.Current research in neurobiology · 2022Review
- Lymphadenopathy at the crossroad between immunodeficiency and autoinflammation: An intriguing challenge.Clinical and experimental immunology · 2021Review
- Article
- Catching viral breast cancer.Infectious agents and cancer · 2021Review
- Epstein-Barr virus peptides derived from latent cycle proteins alter NKG2A + NK cell effector function.Scientific reports · 2020Article
- Proteasomal inhibition triggers viral oncoprotein degradation via autophagy-lysosomal pathway.PLoS pathogens · 2020Article
- Epstein Barr Virus Associated Lymphomas and Epithelia Cancers in Humans.Journal of Cancer · 2020Review
- Mechanisms of B-Cell Oncogenesis Induced by Epstein-Barr Virus.Journal of virology · 2019Review
- Viral-Targeted Strategies Against EBV-Associated Lymphoproliferative Diseases.Frontiers in oncology · 2019Review
- Transcriptional and epigenetic modulation of autophagy promotes EBV oncoprotein EBNA3C induced B-cell survival.Cell death & disease · 2018Article
- Counteracting survival functions of EBNA3C in Epstein-Barr virus (EBV)-driven lymphoproliferative diseases by combination of SAHA and bortezomib.Oncotarget · 2018Article
- Pumilio directs deadenylation-associated translational repression of the cyclin-dependent kinase 1 activator RGC-32.Nucleic acids research · 2018Article
- Therapeutic Strategies against Epstein-Barr Virus-Associated Cancers Using Proteasome Inhibitors.Viruses · 2017Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors.
Funding
Abstract
For over 40 years, EBV infection has been implicated in the etiology of a variety of lymphoid malignancies with the exceptional ability to drive resting B cells to continuously proliferate by successfully overriding cellular apoptotic stimuli. EBV utilizes the normal physiology of B-cell differentiation to persist within the memory B-cell pool of the immunocompetent host and subsequently establishes a life-long latent infection. During latency, out of a subset of viral genes expressed, EBNA-3C is one of the essential antigens required for in vitro primary B-cell transformation. EBNA-3C acts as a transcriptional coregulator by interacting with various cellular and viral factors. For the last 10 years, we have been actively engaged in discerning the biological significance of these interactions and revealed that EBNA-3C primarily targets two important cellular pathways - cell cycle and apoptosis. This review aims to summarize our current knowledge on EBNA-3C-mediated functions and describe how EBNA-3C seizes these cellular pathways that eventually promote B-cell lymphomagenesis. A scrupulous understanding of the critical relationship between EBNA-3C and these cellular machineries will not only aid in elucidating EBV pathogenesis, but also largely facilitate the development of novel diagnostic, as well as therapeutic, strategies against a vast range of EBV-associated B-cell lymphomas.
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What OpenQuestion holds
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.