ArticleJournal of virology2006
Human papillomavirus type 16 E6 activates NF-kappaB, induces cIAP-2 expression, and protects against apoptosis in a PDZ binding motif-dependent manner.
Article in Journal of virology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 81 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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Who cites it
81 citing papers in PubMed, 151 citations in OpenAlex.
- Human papillomavirus and the landscape of secondary genetic alterations in oral cancers.Genome research · 2019Trial
- Cellular signaling in sinecatechins-treated external genital and perianal warts: unraveling the mechanism of action of a botanical therapy.Virologica Sinica · 2015Trial
- Rethinking residual p53 function in HPV-positive cervical cancer cells.Journal of virology · 2026Article
- Human papillomavirus infection and atherosclerotic cardiovascular disease: a comprehensive review of epidemiological evidence, molecular mechanisms, and vaccination-mediated protection.Frontiers in genetics · 2026Review
- Single-cell transcriptomic analysis of HPV-related multiphenotypic sinonasal carcinoma uncovers MYB-HPV association.NPJ precision oncology · 2025Article
- Structural and Functional Insights into Viral and Fungal Proteins Involved in Chronic Inflammation and Their Biologic Treatments.Pharmaceutics · 2025Review
- Exploring the potential link between human papillomavirus infection and coronary artery disease: a review of shared pathways and mechanisms.Molecular and cellular biochemistry · 2025Review
- FXR activation suppresses NF-κB signaling, proliferation and migration in cervical cancer cells.Translational cancer research · 2025Article
- The role of NF-κB in carcinogenesis of cervical cancer: opportunities and challenges.Molecular biology reports · 2024Review
- Do or Die: HPV E5, E6 and E7 in Cell Death Evasion.Pathogens (Basel, Switzerland) · 2022Review
- Article
- HnRNP D activates production of HPV16 E1 and E6 mRNAs by promoting intron retention.Nucleic acids research · 2022Article
- Human Papillomaviruses as Infectious Agents in Gynecological Cancers. Oncogenic Properties of Viral Proteins.International journal of molecular sciences · 2022Review
- Aplysia Neurons as a Model of Alzheimer's Disease: Shared Genes and Differential Expression.Journal of molecular neuroscience : MN · 2022Article
- High-sensitivity C-reactive Protein and Regression of Low-grade Squamous Intraepithelial Lesion: The Role of Low-grade Inflammation in Cervical Carcinogenesis.Journal of epidemiology · 2021Article
- Human papillomavirus E6 and E7: What remains?Tumour virus research · 2021Review
- Inhibition of kinase IKKβ suppresses cellular abnormalities induced by the human papillomavirus oncoprotein HPV 18E6.Scientific reports · 2021Article
- IAP-1 promoted cisplatin resistance in nasopharyngeal carcinoma via inhibition of caspase-3-mediated apoptosis.American journal of cancer research · 2021Article
- Molecular Mechanisms of Exercise on Cancer: A Bibliometrics Study and Visualization AnalysisFrontiers in molecular biosciences · 2021Review
- Co-expression analysis identifies neuro-inflammation as a driver of sensory neuron aging in Aplysia californica.PloS one · 2021Article
21 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 at 2 institutions in 1 country.
Funding
Abstract
Infection with human papillomavirus (HPV) is a critical factor in the pathogenesis of most cervical cancers and some aerodigestive cancers. The HPV E6 oncoprotein from high-risk HPV types contributes to the immortalization and transformation of cells by multiple mechanisms, including degradation of p53, transcriptional activation of human telomerase reverse transcriptase (hTERT), and degradation of several proteins containing PDZ domains. The ability of E6 to bind PDZ domain-containing proteins is independent of p53 degradation or hTERT activation but does correlate with oncogenic potential (R. A. Watson, M. Thomas, L. Banks, and S. Roberts, J. Cell Sci. 116:4925-4934, 2003) and is essential for induction of epithelial hyperplasia in vivo (M. L. Nguyen, M. M. Nguyen, D. Lee, A. E. Griep, and P. F. Lambert, J. Virol. 77:6957-6964, 2003). In this study, we found that HPV type 16 E6 was able to activate NF-kappaB in airway epithelial cells through the induction of nuclear binding activity of p52-containing NF-kappaB complexes in a PDZ binding motif-dependent manner. Transcript accumulation for the NF-kappaB-responsive antiapoptotic gene encoding cIAP-2 and binding of nuclear factors to the proximal NF-kappaB binding site of the cIAP-2 gene promoter are induced by E6 expression. Furthermore, E6 is able to protect cells from TNF-induced apoptosis. All of these E6-dependent phenotypes are dependent on the presence of the PDZ binding motif of E6. Our results imply a role for targeting of PDZ proteins by E6 in NF-kappaB activation and protection from apoptosis in airway epithelial cells.
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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.