ArticleJournal of virology2002
A mutant of human papillomavirus type 16 E6 deficient in binding alpha-helix partners displays reduced oncogenic potential in vivo.
Article in Journal of virology, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 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
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Who cites it
31 citing papers in PubMed, 60 citations in OpenAlex.
- 9-oxo-ODAs suppresses the proliferation of human cervical cancer cells through the inhibition of CDKs and HPV oncoproteins.Scientific reports · 2023Article
- Protein-DNA Interactions Regulate Human Papillomavirus DNA Replication, Transcription, and Oncogenesis.International journal of molecular sciences · 2023Review
- HPV upregulates MARCHF8 ubiquitin ligase and inhibits apoptosis by degrading the death receptors in head and neck cancer.PLoS pathogens · 2023Article
- Human Papillomaviruses as Infectious Agents in Gynecological Cancers. Oncogenic Properties of Viral Proteins.International journal of molecular sciences · 2022Review
- Role of HPV16 E1 in cervical carcinogenesis.Frontiers in cellular and infection microbiology · 2022Review
- The Not-So-Good, the Bad and the Ugly: HPV E5, E6 and E7 Oncoproteins in the Orchestration of Carcinogenesis.Viruses · 2021Review
- Human Papillomavirus E6 and E7: The Cervical Cancer Hallmarks and Targets for Therapy.Frontiers in microbiology · 2019Review
- High-Risk Human Papillomaviral Oncogenes E6 and E7 Target Key Cellular Pathways to Achieve Oncogenesis.International journal of molecular sciences · 2018Review
- Post-Transcriptional Regulation of KLF4 by High-Risk Human Papillomaviruses Is Necessary for the Differentiation-Dependent Viral Life Cycle.PLoS pathogens · 2016Article
- Papillomavirus E6 oncoproteins.Virology · 2013Review
- Epigenetic modulation of signal transduction pathways in HPV-associated HNSCC.Otolaryngology--head and neck surgery : official journal of American Academy of Otolaryngology-Head and Neck Surgery · 2013Article
- Article
- Molecular characterization of head and neck cancer: how close to personalized targeted therapy?Molecular diagnosis & therapy · 2012Article
- Human papillomavirus outcomes in an access-to-care laryngeal cancer cohort.Otolaryngology--head and neck surgery : official journal of American Academy of Otolaryngology-Head and Neck Surgery · 2012Article
- Regulation of the human papillomavirus type 18 E6/E6AP ubiquitin ligase complex by the HECT domain-containing protein EDD.Journal of virology · 2011Article
- GRIM-19 disrupts E6/E6AP complex to rescue p53 and induce apoptosis in cervical cancers.PloS one · 2011Article
- Article
- Human papillomavirus type 16 E6 and E7 oncoproteins act synergistically to cause head and neck cancer in mice.Virology · 2010Article
- Gene expression profile of cervical and skin tissues from human papillomavirus type 16 E6 transgenic mice.BMC cancer · 2008Article
- HPV E6, E6AP and cervical cancer.BMC biochemistry · 2008Review
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Human papillomaviruses (HPVs) are small DNA tumor viruses that are the causative agent of warts and are associated with many anogenital cancers. The viral gene encoding the E6 protein has been found to be involved in HPV oncogenesis. E6 is known to inactivate the cellular tumor suppressor, p53. In addition, E6 has been shown to bind to a variety of other cellular proteins. The focus of this study was to determine what role the interactions of E6 with a subset of cellular proteins which contain a common alpha-helical domain in their E6 binding region (alpha-helix partners) play in E6-mediated phenotypes. We generated transgenic mice expressing a mutant of E6, E6(I128T), which is defective for binding at least a subset of the alpha-helix partners, including E6AP, the ubiquitin ligase that mediates E6-dependent degradation of the p53 protein, to determine whether binding of alpha-helix partners plays a role in E6-mediated activities in vivo. Unlike mice expressing the wild-type E6 (strain K14E6(WT)), the mice expressing E6(I128T) lacked the ability to alter the radiation-induced block to DNA synthesis and promote the formation of benign skin tumors in conjunction with chemical carcinogens. Additionally, they displayed reduced levels of skin hyperplasia, spontaneous skin tumors, and tumor progression activity compared to those of the K14E6(WT) mice. From these results, we conclude that a domain in E6 that mediates alpha-helix partner binding is critical for E6-induced phenotypes in transgenic mice.
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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.