ArticleJournal of virology2005
Role of the E1--E4 protein in the differentiation-dependent life cycle of human papillomavirus type 31.
Article in Journal of virology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 64 papers.
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Who cites it
64 citing papers in PubMed.
- Article
- Differentiation-independent Activation of HPV Genome Replication by the lncRNA DINO.bioRxiv : the preprint server for biology · 2026Article
- Article
- Inhibition of high risk HPV31 E8^E2 repressor activity enables differentiation-independent genome amplification and E4 expression.PLoS pathogens · 2026Article
- Article
- HPV18 L1 and long control region sequences variation and E6/E7 differential expression in nasopharyngeal and cervical cancers: a comparative study.Infectious agents and cancer · 2023Article
- Review
- Review
- Expression of E4 Protein and HPV Major Capsid Protein (L1) as A Novel Combination in Squamous Intraepithelial Lesions.Biomedicines · 2023Article
- Like Brothers in Arms: How Hormonal Stimuli and Changes in the Metabolism Signaling Cooperate, Leading HPV Infection to Drive the Onset of Cervical Cancer.International journal of molecular sciences · 2022Review
- Restriction of viral gene expression and replication prevents immortalization of human keratinocytes by a beta-human papillomavirus.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- The Induced Expression ofInternational journal of molecular sciences · 2022Article
- Human Papillomaviruses as Infectious Agents in Gynecological Cancers. Oncogenic Properties of Viral Proteins.International journal of molecular sciences · 2022Review
- Epigenetic and Transcriptomic Regulation Landscape in HPV+ Cancers: Biological and Clinical Implications.Frontiers in genetics · 2022Review
- The chromatin insulator CTCF regulates HPV18 transcript splicing and differentiation-dependent late gene expression.PLoS pathogens · 2021Article
- Human Papillomaviruses Target the DNA Damage Repair and Innate Immune Response Pathways to Allow for Persistent Infection.Viruses · 2021Review
- Review
- Inferring Virus-Host relationship between HPV and its host Homo sapiens using protein interaction network.Scientific reports · 2020Article
- Intrinsically disordered proteins of viruses: Involvement in the mechanism of cell regulation and pathogenesis.Progress in molecular biology and translational science · 2020Review
- Roles for E1-independent replication and E6-mediated p53 degradation during low-risk and high-risk human papillomavirus genome maintenance.PLoS pathogens · 2019Article
4 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors.
Funding
Abstract
The most highly expressed protein in the productive life cycle of human papillomaviruses (HPVs) is E1--E4, but its function is not well understood. To investigate the role of E1--E4, we undertook a genetic analysis in the context of the complete HPV type 31 (HPV31) genome. A mutant HPV31 genome (E4M9) was constructed that contained a stop codon in the E4 open reading frame at amino acid 9 and was silent in the overlapping E2 coding sequence. Wild-type and mutant genomes were transfected into normal human foreskin keratinocytes (HFKs) and selected for drug resistance, and pooled cultures were examined for effects of E1--E4 on viral functions. Southern blot analyses of transfected HFKs demonstrated that cells carrying the E4M9 mutant genomes were maintained as episomes at copy numbers similar to those in keratinocytes transfected with wild-type HPV31. Both sets of cells grew at similar rates, exhibited comparable extensions of life spans, and had equivalent levels of early transcripts. Following suspension of the cells in a semisolid medium, differentiation-dependent genome amplification and late gene expression were significantly decreased in cells maintaining the E4M9 mutant genome compared to those with wild-type HPV31. One explanation for these effects could be a reduction in the number of cells harboring mutant genomes that enter S phase upon differentiation. An analysis of cells containing E4M9 mutant genomes in organotypic raft cultures indicated a reduction in bromodeoxyuridine incorporation in differentiated suprabasal cells compared to that seen in wild-type rafts. Our results indicate that the HPV31 E1--E4 protein plays a significant role in promoting HPV genome amplification and S phase maintenance during differentiation.
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