ArticleVirus research2009
Modulation of JC virus transcription by C/EBPbeta.
Article in Virus research, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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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.
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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
29 citing papers in PubMed, 38 citations in OpenAlex.
- Genetic Diversity of the Polyomavirus JC and Implications for the Pathogenesis of Progressive Multifocal Leukoencephalopathy.Viruses · 2026Review
- Molecular characterization of JC virus in progressive multifocal leukoencephalopathy cases from India.Scientific reports · 2025Article
- Electrophoretic Mobility Shift Assay for Identification of the Interaction Between a Viral Protein and DNA.Methods in molecular biology (Clifton, N.J.) · 2025Article
- Article
- Rearrangement in the Hypervariable Region of JC Polyomavirus Genomes Isolated from Patient Samples and Impact on Transcription Factor-Binding Sites and Disease Outcomes.International journal of molecular sciences · 2022Article
- Article
- Review
- The Role of the JC Virus in Central Nervous System Tumorigenesis.International journal of molecular sciences · 2020Review
- The DNA damage response promotes polyomavirus JC infection by nucleus to cytoplasm NF- kappaB activation.Virology journal · 2017Article
- The Brd4 acetyllysine-binding protein is involved in activation of polyomavirus JC.Journal of neurovirology · 2016Article
- Expression of Signaling Molecules in Progressive Multifocal Leukoencephalopathy.Current HIV research · 2016Article
- Animal Models for Progressive Multifocal Leukoencephalopathy.Journal of cellular physiology · 2015Review
- Epigenetic regulation of polyomavirus JC involves acetylation of specific lysine residues in NF-κB p65.Journal of neurovirology · 2015Article
- Persistence and pathogenesis of the neurotropic polyomavirus JC.Annals of neurology · 2015Review
- Degradation of polyomavirus JC T-antigen by stress involves the LIP isoform of C/EBP.Cell cycle (Georgetown, Tex.) · 2015Article
- Reactivation of human polyomaviruses in immunocompromised states.Journal of neurovirology · 2014Article
- Rad51 activates polyomavirus JC early transcription.PloS one · 2014Article
- The T antigen locus of Merkel cell polyomavirus downregulates human Toll-like receptor 9 expression.Journal of virology · 2013Article
- Epigenetic regulation of polyomavirus JC.Virology journal · 2013Article
- The rapidly expanding family of human polyomaviruses: recent developments in understanding their life cycle and role in human pathology.PLoS pathogens · 2013Review
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
The polyomavirus JC (JCV) causes the demyelinating disease progressive multifocal leukoencephalopathy (PML). Infection by JCV is very common in childhood after which the virus enters a latent state, which is poorly understood. Under conditions of severe immunosuppression, especially AIDS, JCV may reactivate to cause PML. Expression of JC viral proteins is regulated by the JCV non-coding control region (NCCR), which contains an NF-kappaB binding site previously shown to activate transcription. We now report that C/EBPbeta inhibits basal and NF-kappaB-stimulated JCV transcription via the same site. Gel shift analysis showed C/EBPbeta bound to this region in vitro and ChIP assays confirmed this binding in vivo. Further, a ternary complex of NF-kappaB/p65, C/EBPbeta-LIP and JCV DNA could be detected in co-immunoprecipitation experiments. Mutagenesis analysis of the JCV NCCR indicated p65 and C/EBPbeta-LIP bound to adjacent but distinct sites and that both sites regulate basal and p65-stimulated transcription. Thus C/EBPbeta negatively regulates JCV, which together with NF-kappaB activation, may control the balance between JCV latency and activation leading to PML. This balance may be regulated by proinflammatory cytokines in the brain.
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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.