ArticleJournal of virology2022
Loss of the E6AP Ubiquitin Ligase Induces p53-Dependent Phosphorylation of Human Papillomavirus 18 E6 in Cells Derived from Cervical Cancer.
Article in Journal of virology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 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
8 citing papers in PubMed, 11 citations in OpenAlex.
- Differential roles of type I topoisomerases in regulating HPV pathogenesis.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- The Role of HPV and Hormone in Cervical Precancer and Cancer: Molecular Pathophysiology and Cell Biology of Disease and Treatment.Oncology research · 2026Review
- Molecular Insights into HPV-Driven Cervical Cancer: Oncoproteins, Immune Evasion, and Epigenetic Modifications.Microorganisms · 2025Review
- Activating transcription factor 3 induces oxidative stress and genotoxicity, transcriptionally modulating metastasis-related gene expression in human papillomavirus-infected cervical cancer.Virology journal · 2025Article
- E6AP is essential for the proliferation of HPV-positive cancer cells by preventing senescence.PLoS pathogens · 2025Article
- Review
- Regulation of HPV E7 Stability by E6-Associated Protein (E6AP).Journal of virology · 2022Article
- Molecular Mechanisms of HIV Protease Inhibitors Against HPV-Associated Cervical Cancer: Restoration ofFrontiers in molecular biosciences · 2022Review
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cancer-causing human papillomavirus (HPV) E6 oncoproteins contain a well-characterized phosphoacceptor site within the PDZ (PSD-95/Dlg/ZO-1) binding motif (PBM) at the C terminus of the protein. Previous studies have shown that the threonine or serine residue in the E6 PBM is subject to phosphorylation by several stress-responsive cellular kinases upon the induction of DNA damage in cervical cancer-derived cells. However, there is little information about the regulation of E6 phosphorylation in the absence of DNA damage and whether there may be other pathways by which E6 is phosphorylated. In this study, we demonstrate that loss of E6AP results in a dramatic increase in the levels of phosphorylated E6 (pE6) despite the expected overall reduction in total E6 protein levels. Furthermore, phosphorylation of E6 requires transcriptionally active p53 and occurs in a manner that is dependent upon DNA-dependent protein kinase (DNA PK). These results identify a novel feedback loop, where loss of E6AP results in upregulation of p53, leading to increased levels of E6 phosphorylation, which in turn correlates with increased association with 14-3-3 and inhibition of p53 transcriptional activity.
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.