ArticleJournal of virology2008
hAda3 degradation by papillomavirus type 16 E6 correlates with abrogation of the p14ARF-p53 pathway and efficient immortalization of human mammary epithelial cells.
Article in Journal of virology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 26 citations in OpenAlex.
- The Hallmarks of Cervical Cancer: Molecular Mechanisms Induced by Human Papillomavirus.Biology · 2024Review
- HPV upregulates MARCHF8 ubiquitin ligase and inhibits apoptosis by degrading the death receptors in head and neck cancer.PLoS pathogens · 2023Article
- The C-Terminal Domain of NefVaccines · 2021Article
- Comparative molecular profiling of HPV-induced squamous cell carcinomas.Cancer medicine · 2017Article
- ADA3 regulates normal and tumor mammary epithelial cell proliferation through c-MYC.Breast cancer research : BCR · 2016Article
- Tale of a multifaceted co-activator, hADA3: from embryogenesis to cancer and beyond.Open biology · 2016Review
- Molecular Probing of the HPV-16 E6 Protein Alpha Helix Binding Groove with Small Molecule Inhibitors.PloS one · 2016Article
- Human papillomavirus molecular biology and disease association.Reviews in medical virology · 2015Review
- Manipulation of cellular DNA damage repair machinery facilitates propagation of human papillomaviruses.Seminars in cancer biology · 2014Review
- Article
- Papillomavirus E6 oncoproteins.Virology · 2013Review
- Genomic instability: Ada3 and HPV E6-acetyltransferase connections?Cell cycle (Georgetown, Tex.) · 2013Article
- Virology and molecular pathogenesis of HPV (human papillomavirus)-associated oropharyngeal squamous cell carcinoma.The Biochemical journal · 2012Review
- Article
- Papillomavirus E6 proteins.Virology · 2009Review
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Two activities of human papillomavirus type 16 E6 (HPV16 E6) are proposed to contribute to the efficient immortalization of human epithelial cells: the degradation of p53 protein and the induction of telomerase. However, the requirement for p53 inactivation has been debated. Another E6 target is the hAda3 protein, a p53 coactivator and a component of histone acetyltransferase complexes. We have previously described the role of hAda3 and p53 acetylation in p14ARF-induced human mammary epithelial cell (MEC) senescence (P. Sekaric, V. A. Shamanin, J. Luo, and E. J. Androphy, Oncogene 26:6261-6268, 2007). In this study, we analyzed a set of HPV16 E6 mutants for the ability to induce hAda3 degradation. E6 mutants that degrade hAda3 but not p53 could abrogate p14ARF-induced growth arrest despite the presence of normal levels of p53 and efficiently immortalized MECs. However, two E6 mutants that previously were reported to immortalize MECs with low efficiency were found to be defective for both p53 and hAda3 degradation. We found that these immortal MECs select for reduced p53 protein levels through a proteasome-dependent mechanism. The findings strongly imply that the inactivation of the p14ARF-p53 pathway, either by the E6-mediated degradation of p53 or hAda3 or by cellular adaptation, is required for MEC immortalization.
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Registered trials
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