ArticleJournal of cell science2010
E1--E4-mediated keratin phosphorylation and ubiquitylation: a mechanism for keratin depletion in HPV16-infected epithelium.
Article in Journal of cell science, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 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
25 citing papers in PubMed.
- Human papilloma virus (HPV) mediated cancers: an insightful update.Journal of translational medicine · 2025Review
- Molecular Insights into HPV-Driven Cervical Cancer: Oncoproteins, Immune Evasion, and Epigenetic Modifications.Microorganisms · 2025Review
- How human papillomavirus (HPV) targets DNA repair pathways for viral replication: from guardian to accomplice.Microbiology and molecular biology reviews : MMBR · 2025Review
- Navigating therapeutic strategies: HPV classification in head and neck cancer.British journal of cancer · 2024Review
- Alternative splicing in the genome of HPV and its regulation.Frontiers in cellular and infection microbiology · 2024Review
- Epidemiology and Molecular Biology of HPV Variants in Cervical Cancer: The State of the Art in Mexico.International journal of molecular sciences · 2022Review
- HPV16 and HPV18 Genome Structure, Expression, and Post-Transcriptional Regulation.International journal of molecular sciences · 2022Review
- Human Papillomaviruses as Infectious Agents in Gynecological Cancers. Oncogenic Properties of Viral Proteins.International journal of molecular sciences · 2022Review
- WJ‑MSCs intervention may relieve intrauterine adhesions in female rats via TGF‑β1‑mediated Rho/ROCK signaling inhibition.Molecular medicine reports · 2021Article
- Keratin 6a reorganization for ubiquitin-proteasomal processing is a direct antimicrobial response.The Journal of cell biology · 2018Article
- Mechanisms by which HPV Induces a Replication Competent Environment in Differentiating Keratinocytes.Viruses · 2017Review
- Intracellular Motility of Intermediate Filaments.Cold Spring Harbor perspectives in biology · 2017Review
- Article
- Potential Role of E4 Protein in Human Papillomavirus Screening: a ReviewAsian Pacific journal of cancer prevention : APJCP · 2017Review
- Review
- Endoplasmic Reticulum: The Favorite Intracellular Niche for Viral Replication and Assembly.Viruses · 2016Review
- Review
- Human papillomavirus type 1 E1^E4 protein is a potent inhibitor of the serine-arginine (SR) protein kinase SRPK1 and inhibits phosphorylation of host SR proteins and of the viral transcription and replication regulator E2.Journal of virology · 2014Article
- The role of ubiquitin and ubiquitin-like modification systems in papillomavirus biology.Viruses · 2014Review
- Modulation of apoptotic pathways by human papillomaviruses (HPV): mechanisms and implications for therapy.Viruses · 2012Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors.
Funding
Abstract
The keratin IF network of epidermal keratinocytes provides a protective barrier against mechanical insult, it is also a major player in absorbing stress in these cells. The human papilloma virus (HPV) type 16 E1--E4 protein accumulates in the upper layers of HPV16-infected epithelium and is known to associate with and reorganise the keratin IF network in cells in culture. Here, we show that this function is conserved amongst a number of HPV alpha-group E1--E4 proteins and that the differentiation-dependent keratins are also targeted. Using time-lapse microscopy, HPV16 E1--E4 was found to effect a dramatic cessation of keratin IF network dynamics by associating with both soluble and insoluble keratin. Network disruption was accompanied by keratin hyperphosphorylation at several sites, including K8 S73, which is typically phosphorylated in response to stress stimuli. Keratin immunoprecipitated from E1--E4-expressing cells was also found to be ubiquitylated, indicating that it is targeted for proteasomal degradation. Interestingly, the accumulation of hyperphosphorylated, ubiquitylated E1--E4-keratin structures was found to result in an impairment of proteasomal function. These observations shed new light on the mechanism of keratin IF network reorganisation mediated by HPV16 E1--E4 and provide an insight into the depletion of keratin co-incident with E1--E4 accumulation observed in HPV-infected epithelium.
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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.