ArticleJournal of virology2004
Cyclin/CDK regulates the nucleocytoplasmic localization of the human papillomavirus E1 DNA helicase.
Article in Journal of virology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 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.
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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.
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Who cites it
41 citing papers in PubMed, 80 citations in OpenAlex.
- HPV16 E2 protein possesses intrinsic helicase activity and sterically hinders E1 function through direct interaction.The Journal of biological chemistry · 2026Article
- Molecular Insights into HPV-Driven Cervical Cancer: Oncoproteins, Immune Evasion, and Epigenetic Modifications.Microorganisms · 2025Review
- Deciphering the divergent transcriptomic landscapes of cervical cancer cells grown in 3D and 2D cell culture systems.Frontiers in cell and developmental biology · 2024Article
- Review
- Review
- Activity of CK2α protein kinase is required for efficient replication of some HPV types.PLoS pathogens · 2019Article
- Cottontail Rabbit Papillomavirus E1 and E2 Proteins Mutually Influence Their Subcellular Localizations.Journal of virology · 2018Article
- Mechanisms by which HPV Induces a Replication Competent Environment in Differentiating Keratinocytes.Viruses · 2017Review
- Host cell restriction factors that limit transcription and replication of human papillomavirus.Virus research · 2017Review
- Article
- Synthetic lethal mutations in the cyclin A interface of human cytomegalovirus.PLoS pathogens · 2017Article
- Cellular Model of p21-Induced Senescence.Methods in molecular biology (Clifton, N.J.) · 2017Article
- Phosphorylation of bovine papillomavirus E1 by the protein kinase CK2 near the nuclear localization signal does not influence subcellular distribution of the protein in dividing cells.Archives of virology · 2016Article
- Human papillomavirus molecular biology and disease association.Reviews in medical virology · 2015Review
- Replication interference between human papillomavirus types 16 and 18 mediated by heterologous E1 helicases.Virology journal · 2014Article
- The E1 proteins.Virology · 2013Review
- Human papillomavirus infections: warts or cancer?Cold Spring Harbor perspectives in biology · 2013Review
- CK2 phosphorylation inactivates DNA binding by the papillomavirus E1 and E2 proteins.Journal of virology · 2013Article
- Targeting human papillomavirus genome replication for antiviral drug discovery.Antiviral therapy · 2013Review
- Engagement of the ATR-dependent DNA damage response at the human papillomavirus 18 replication centers during the initial amplification.Journal of virology · 2013Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
Cyclin-dependent kinases (CDKs) play key roles in eukaryotic DNA replication and cell cycle progression. Phosphorylation of components of the preinitiation complex activates replication and prevents reinitiation. One mechanism is mediated by nuclear export of critical proteins. Human papillomavirus (HPV) DNA replication requires cellular machinery in addition to the viral replicative DNA helicase E1 and origin recognition protein E2. E1 phosphorylation by cyclin/CDK is critical for efficient viral DNA replication. We now show that E1 is phosphorylated by CDKs in vivo and that phosphorylation regulates its nucleocytoplasmic localization. We identified a conserved regulatory region for localization which contains a dominant leucine-rich nuclear export sequence (NES), the previously defined cyclin binding motif, three serine residues that are CDK substrates, and a putative bipartite nuclear localization sequence. We show that E1 is exported from the nucleus by a CRM1-dependent mechanism unless the NES is inactivated by CDK phosphorylation. Replication activities of E1 phosphorylation site mutations are reduced and correlate inversely with their increased cytoplasmic localization. Nuclear localization and replication activities of most of these mutations are enhanced or restored by mutations in the NES. Collectively, our data demonstrate that CDK phosphorylation controls E1 nuclear localization to support viral DNA amplification. Thus, HPV adopts and adapts the cellular regulatory mechanism to complete its reproductive program.
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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.