ArticleJournal of virology2009
The human papillomavirus (HPV) E6* proteins from high-risk, mucosal HPVs can direct degradation of cellular proteins in the absence of full-length E6 protein.
Article in Journal of virology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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Who cites it
31 citing papers in PubMed, 59 citations in OpenAlex.
- New mouse model based on adenocarcinoma 4T1 cells expressing HPV16 E6 and E7 applied to assess the efficacy of therapeutic and prophylactic E6/E7-based HPV16 vaccines.Infectious agents and cancer · 2025Article
- Article
- HPV E6/E7: insights into their regulatory role and mechanism in signaling pathways in HPV-associated tumor.Cancer gene therapy · 2024Review
- Alternative splicing in the genome of HPV and its regulation.Frontiers in cellular and infection microbiology · 2024Review
- Observational
- PDZ Domain-Containing Protein NHERF-2 Is a Novel Target of Human Papillomavirus 16 (HPV-16) and HPV-18.Journal of virology · 2019Article
- PDZ Domains as Drug Targets.Advanced therapeutics · 2019Review
- Comparative RNA sequencing reveals that HPV16 E6 abrogates the effect of E6*I on ROS metabolism.Scientific reports · 2019Article
- E6/E7 and E6Frontiers in immunology · 2019Article
- HPV-18 E6 Oncoprotein and Its Spliced Isoform E6*I Regulate the Wnt/β-Catenin Cell Signaling Pathway through the TCF-4 Transcriptional Factor.International journal of molecular sciences · 2018Article
- A quantitative LumiFluo assay to test inhibitory compounds blocking p53 degradation induced by human papillomavirus oncoprotein E6 in living cells.Scientific reports · 2018Article
- Review
- Comparative analysis of HPV16 gene expression profiles in cervical and in oropharyngeal squamous cell carcinoma.Oncotarget · 2017Article
- Viral Interactions with PDZ Domain-Containing Proteins-An Oncogenic Trait?Pathogens (Basel, Switzerland) · 2016Review
- Human Papillomavirus: Current and Future RNAi Therapeutic Strategies for Cervical Cancer.Journal of clinical medicine · 2015Review
- The role of the PI3K/Akt/mTOR signalling pathway in human cancers induced by infection with human papillomaviruses.Molecular cancer · 2015Review
- Article
- Oncogenes and RNA splicing of human tumor viruses.Emerging microbes & infections · 2014Review
- The small splice variant of HPV16 E6, E6, reduces tumor formation in cervical carcinoma xenografts.Virology · 2014Article
- Papillomavirus E6 oncoproteins.Virology · 2013Review
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The E6 oncoproteins from high-risk mucosotrophic human papillomaviruses (HPVs) target a range of cellular proteins for proteasome-mediated degradation. Apart from the tumor suppressor p53 and proapoptotic Bcl-2 family member Bak, many targets contain class 1 PDZ domains and are involved in cell junction stability and signaling. The targeting mechanism is considered to function by the E6 protein acting as an adaptor molecule linking a cellular ubiquitin ligase to the target protein. In each case, whether the target is the p53 tumor suppressor or a member of the group of PDZ domain-containing targets, this mechanism relies on a direct interaction between E6 and its cellular target. This study focuses on the impact of the HPV type 18 (HPV-18) E6*I protein on the stability of Akt, Dlg, MAGI-1, MAGI-2, and Scribble. We show that HPV-18 E6* expression can downregulate the expression levels of Akt, Dlg, and Scribble in the absence of full-length HPV-18 E6 protein. The reduction in Dlg levels by E6* is independent of transcription and does not require a direct interaction between the two proteins although the proteasome pathway is involved. Further, we provide evidence that activation of certain signal transduction pathways has a profound effect on the targeting of Dlg by E6* and suggest that high-risk HPV E6 oncoproteins can target certain substrates both directly and indirectly through the E6* proteins and may cooperate in their degradation.
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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.