ArticlePLoS pathogens2013
Inactivation of p53 rescues the maintenance of high risk HPV DNA genomes deficient in expression of E6.
Article in PLoS pathogens, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 28 citations in OpenAlex.
- The p53 DNA-Binding (Core) Domain can form a prion that seeds prion formation in full-length p53.Microbial cell (Graz, Austria) · 2026Article
- Commensal papillomavirus immunity preserves the homeostasis of highly mutated normal skin.Cancer cell · 2025Article
- Single cell transcriptomic analysis of HPV16-infected epithelium identifies a keratinocyte subpopulation implicated in cancer.Nature communications · 2023Article
- Loss of the E6AP Ubiquitin Ligase Induces p53-Dependent Phosphorylation of Human Papillomavirus 18 E6 in Cells Derived from Cervical Cancer.Journal of virology · 2022Article
- Regulation of Human Papillomavirus 18 Genome Replication, Establishment, and Persistence by Sequences in the Viral Upstream Regulatory Region.Journal of virology · 2021Article
- Persistent Human Papillomavirus Infection.Viruses · 2021Review
- Genomic and phylogenetic characterization of ChPV2, a novel goat PV closely related to the Xi-PV1 species infecting bovines.Virology journal · 2020Article
- Roles for E1-independent replication and E6-mediated p53 degradation during low-risk and high-risk human papillomavirus genome maintenance.PLoS pathogens · 2019Article
- Article
- Mucosal and Cutaneous Human Papillomavirus Infections and Cancer Biology.Frontiers in oncology · 2019Review
- The Human Papillomavirus E6 PDZ Binding Motif Links DNA Damage Response Signaling to E6 Inhibition of p53 Transcriptional Activity.Journal of virology · 2018Article
- STAT3 activation by E6 is essential for the differentiation-dependent HPV18 life cycle.PLoS pathogens · 2018Article
- Human Papillomavirus E6 interaction with cellular PDZ domain proteins modulates YAP nuclear localization.Virology · 2018Article
- Host cell restriction factors that limit transcription and replication of human papillomavirus.Virus research · 2017Review
- Human papillomavirus promotes Epstein-Barr virus maintenance and lytic reactivation in immortalized oral keratinocytes.Virology · 2016Article
- Using Organotypic Epithelial Tissue Culture to Study the Human Papillomavirus Life Cycle.Current protocols in microbiology · 2016Article
- The Deacetylase Sirtuin 1 Regulates Human Papillomavirus Replication by Modulating Histone Acetylation and Recruitment of DNA Damage Factors NBS1 and Rad51 to Viral Genomes.PLoS pathogens · 2015Article
- Review
- Cancer-causing human papillomavirus E6 proteins display major differences in the phospho-regulation of their PDZ interactions.Journal of virology · 2015Article
- Human Papillomavirus (HPV) Prevalence in Nasal and Antrochoanal Polyps and Association with Clinical Data.PloS one · 2015Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
The human papillomavirus DNA genome undergoes three distinct stages of replication: establishment, maintenance and amplification. We show that the HPV16 E6 protein is required for the maintenance of the HPV16 DNA genome as an extrachromosomal, nuclear plasmid in its natural host cell, the human keratinocyte. Based upon mutational analyses, inactivation of p53 by E6, but not necessarily E6-mediated degradation of p53, was found to correlate with the ability of E6 to support maintenance of the HPV16 genome as a nuclear plasmid. Inactivation of p53 with dominant negative p53 rescued the ability of HPV16 E6STOP and E6SAT mutant genomes to replicate as extrachromosomal genomes, though not to the same degree as observed for the HPV16 E6 wild-type (WT) genome. Inactivation of p53 also rescued the ability of HPV18 and HPV31 E6-deficient genomes to be maintained at copy numbers comparable to that of HPV18 and HPV31 E6WT genomes at early passages, though upon further passaging copy numbers for the HPV18 and 31 E6-deficient genomes lessened compared to that of the WT genomes. We conclude that inactivation of p53 is necessary for maintenance of HPV16 and for HPV18 and 31 to replicate at WT copy number, but that additional functions of E6 independent of inactivating p53 must also contribute to the maintenance of these genomes. Together these results suggest that re-activation of p53 may be a possible means for eradicating extrachromosomal HPV16, 18 or 31 genomes in the context of persistent infections.
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