ArticleNature2010
Heterochromatin silencing of p53 target genes by a small viral protein.
Article in Nature, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 85 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
85 citing papers in PubMed, 121 citations in OpenAlex.
- The FACT complex associates with the RPA complex at viral replication compartments to promote adenovirus infection.Journal of virology · 2026Article
- The adenovirus oncoprotein E1B-55K reshapes epigenetic histone modifications in primary human cells.mBio · 2026Article
- Genome-replicating HC-AdV: A novel high-capacity adenoviral vector class featuring enhancedMolecular therapy. Methods & clinical development · 2025Article
- Cellular transcription factor TFII-I represses adenovirus gene expression.Journal of virology · 2025Article
- Article
- Expanding the adenovirus toolbox: reporter viruses for studying the dynamics of human adenovirus replication.Journal of virology · 2024Article
- Virus-induced host genomic remodeling dysregulates gene expression, triggering tumorigenesis.Frontiers in cellular and infection microbiology · 2024Review
- (E1)levating COVID-19 vaccine efficiency with adenoviral E1 proteins.Science advances · 2022Review
- Metabolic Control by DNA Tumor Virus-Encoded Proteins.Pathogens (Basel, Switzerland) · 2021Review
- Emerging antiviral therapeutics for human adenovirus infection: Recent developments and novel strategies.Antiviral research · 2021Review
- Tumor suppressor p53: from engaging DNA to target gene regulation.Nucleic acids research · 2020Article
- Review
- Adenovirus targets transcriptional and posttranslational mechanisms to limit gap junction function.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2020Article
- ATO (Arsenic Trioxide) Effects on Promyelocytic Leukemia Nuclear Bodies Reveals Antiviral Intervention Capacity.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2020Article
- Epigenetics and the dynamics of chromatin during adenovirus infections.FEBS letters · 2019Review
- Adenoviral strategies to overcome innate cellular responses to infection.FEBS letters · 2019Review
- Adenovirus 5 E1A Interacts with E4orf3 To Regulate Viral Chromatin Organization.Journal of virology · 2019Article
- p53 Isoforms and Their Implications in Cancer.Cancers · 2018Review
- Adenovirus 5 E1A-Mediated Suppression of p53 via FUBP1.Journal of virology · 2018Article
- Human Oncoviruses and p53 Tumor Suppressor Pathway Deregulation at the Origin of Human Cancers.Cancers · 2018Review
25 more citing papers are in PubMed but not listed here.
Corrections and comments
- Commented on by
- Commented on by
- Erratum issued
Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
The transcription factor p53 (also known as TP53) guards against tumour and virus replication and is inactivated in almost all cancers. p53-activated transcription of target genes is thought to be synonymous with the stabilization of p53 in response to oncogenes and DNA damage. During adenovirus replication, the degradation of p53 by E1B-55k is considered essential for p53 inactivation, and is the basis for p53-selective viral cancer therapies. Here we reveal a dominant epigenetic mechanism that silences p53-activated transcription, irrespective of p53 phosphorylation and stabilization. We show that another adenoviral protein, E4-ORF3, inactivates p53 independently of E1B-55k by forming a nuclear structure that induces de novo H3K9me3 heterochromatin formation at p53 target promoters, preventing p53-DNA binding. This suppressive nuclear web is highly selective in silencing p53 promoters and operates in the backdrop of global transcriptional changes that drive oncogenic replication. These findings are important for understanding how high levels of wild-type p53 might also be inactivated in cancer as well as the mechanisms that induce aberrant epigenetic silencing of tumour-suppressor loci. Our study changes the longstanding definition of how p53 is inactivated in adenovirus infection and provides key insights that could enable the development of true p53-selective oncolytic viral therapies.
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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.