ArticleMolecular and cellular biology2013
Altered binding site selection of p53 transcription cassettes by hepatitis B virus X protein.
Article in Molecular and cellular biology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 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
18 citing papers in PubMed, 44 citations in OpenAlex.
- Molecular Basis and Clinical Significance of the High-risk Phenotype of Hepatitis B Virus Genotype C.Journal of clinical and translational hepatology · 2026Review
- Review
- Molecular and Clinical Features of Hepatocellular Carcinoma in Patients with HBV-HDV Infection.Journal of hepatocellular carcinoma · 2023Review
- mTOR Signaling: The Interface Linking Cellular Metabolism and Hepatitis B Virus Replication.Virologica Sinica · 2021Review
- HBP1-mediated transcriptional repression of AFP inhibits hepatoma progression.Journal of experimental & clinical cancer research : CR · 2021Article
- The Hepatitis B Virus Interactome: A Comprehensive Overview.Frontiers in microbiology · 2021Review
- Dysregulation of the cohesin subunit RAD21 by Hepatitis C virus mediates host-virus interactions.Nucleic acids research · 2019Article
- 14-3-3ζ binds to hepatitis B virus protein X and maintains its protein stability in hepatocellular carcinoma cells.Cancer medicine · 2018Article
- Hepatitis B virus-X protein regulates high mobility group box 1 to promote the formation of hepatocellular carcinoma.Oncology letters · 2018Article
- Interference of Apoptosis by Hepatitis B Virus.Viruses · 2017Review
- p53 signaling modulation of cell cycle arrest and viral replication in porcine circovirus type 2 infection cells.Veterinary research · 2016Article
- p53 Loses grip on PIK3CA expression leading to enhanced cell survival during platinum resistance.Molecular oncology · 2016Article
- Global re-wiring of p53 transcription regulation by the hepatitis B virus X protein.Molecular oncology · 2016Article
- Hepatitis B Virus X Protein Driven Alpha Fetoprotein Expression to Promote Malignant Behaviors of Normal Liver Cells and Hepatoma Cells.Journal of Cancer · 2016Article
- Technical standards for hepatitis B virus X protein (HBx) research.Hepatology (Baltimore, Md.) · 2015Review
- Interactions of chromatin context, binding site sequence content, and sequence evolution in stress-induced p53 occupancy and transactivation.PLoS genetics · 2015Article
- Virus associated malignancies: the role of viral hepatitis in hepatocellular carcinoma.Seminars in cancer biology · 2014Review
- Liver-specific expressions of HBx and src in the p53 mutant trigger hepatocarcinogenesis in zebrafish.PloS one · 2013Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The key cellular regulator p53 is a common target of viral oncoproteins. However, the mechanism by which p53 transcription regulation is modulated by hepatitis B virus X protein (HBx), a transcription cofactor implicated in hepatitis B virus-associated hepatocellular carcinoma (HCC), is poorly understood. By integrating p53 chromatin immunoprecipitation (ChIP)-on-chip and expression profiling of an HBx-expressing cell culture system, we report that HBx alters p53 binding site selectivity in the regulatory regions of genes, and this is associated with their aberrant expression. Using an HBx-deregulated gene, p53AIP1, as a model, we show that HBx aberrantly increases p53AIP1 expression by conferring p53 selectivity for a more conserved binding site in its regulatory region. We further demonstrate that HBx-deregulated increased p53AIP1 expression is relevant in HCC livers and define a functional role for p53AIP1 in mediating HBx-induced apoptosis in vitro. Significantly, we provide evidence that specific p53-associated transcription cofactors and coregulators are differentially recruited in the presence of HBx, effecting a PCAF-mediated "p53 Lys320 acetylation switch" that results in altered binding site selection of distinct p53 transcription cassettes. The findings here clarify the role of HBx in modulating p53 transcription regulation and provide a novel mechanistic insight into this deregulation.
Indexed as
Identifiers
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.