Papillomavirus E6 oncoproteins.
TLDR
These E6 protein-complexes, together with other proteins that bind to E6, alter a broad array of biological outcomes including modulation of cell survival, cellular transcription, host cell differentiation, growth factor dependence, DNA damage responses, and cell cycle progression.About:
This article is published in Virology.The article was published on 2013-10-01 and is currently open access. It has received 277 citations till now. The article focuses on the topics: Plasma protein binding & Growth factor.read more
Citations
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Integrated genomic and molecular characterization of cervical cancer
TL;DR: The extensive molecular characterization of 228 primary cervical cancers is reported, one of the largest comprehensive genomic studies of cervical cancer to date, and novel significantly mutated genes in cervical cancer are identified, revealing new potential therapeutic targets for cervical cancers.
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Carcinogenic human papillomavirus infection.
Mark Schiffman,John Doorbar,Nicolas Wentzensen,Silvia de Sanjosé,Carole Fakhry,Bradley J. Monk,Margaret Stanley,Silvia Franceschi +7 more
TL;DR: HPV testing will probably replace cytology-based cervical screening owing to greater reassurance when the test is negative, however, the effective implementation of HPV vaccination and screening globally remains a challenge.
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Human viral oncogenesis: a cancer hallmarks analysis.
TL;DR: The Hallmarks of Cancer framework of Hanahan and Weinberg (2000 and 2011) is used to dissect the viral, host, and environmental cofactors that contribute to the biology of multistep oncogenesis mediated by established human oncoviruses.
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Human Papillomaviruses; Epithelial Tropisms, and the Development of Neoplasia
TL;DR: It appears that cellular environment and the site of infection affect viral pathogenicity by modulating viral gene expression, and changes in E6 and E7 expression are thought to account for the development of neoplasias at the endocervix, the anal and cervical transformation zones, and the tonsilar crypts and other oropharyngeal sites.
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The human papillomavirus family and its role in carcinogenesis.
TL;DR: Additional research is necessary to characterize the biology and epidemiology of the vast number of HPV types that have been poorly investigated so far, with a final aim of clarifying their potential roles in other human diseases.
References
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The E6 oncoprotein encoded by human papillomavirus types 16 and 18 promotes the degradation of p53
TL;DR: It is demonstrated that the E6 proteins of the oncogenic HPVs that bind p53 stimulate the degradation of p53, which results in selective degradation of cellular proteins such as p53 with negative regulatory functions provides a novel mechanism of action for dominant-acting oncoproteins.
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Classification of papillomaviruses
Ethel Michele De Villiers,Claude M. Fauquet,Thomas R. Broker,Hans-Ulrich Bernard,Harald zur Hausen +4 more
TL;DR: The higher-order PV taxonomy is described following the general criteria established by the International Committee on the Taxonomy of Viruses (ICTV), reviews the literature of the lower order taxa, lists all known "PV types", and interprets their phylogenetic relationship.
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Association of human papillomavirus types 16 and 18 E6 proteins with p53.
TL;DR: This study shows that the E6 protein of HPV-16 is capable of binding to the cellular p53 protein, providing further evidence that the human papillomaviruses, the adenovirus type 5, and SV40 may effect similar cellular pathways in transformation.
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The HPV-16 E6 and E6-AP complex functions as a ubiquitin-protein ligase in the ubiquitination of p53
TL;DR: The purification and identification of the factors necessary for the E6-E6-AP-mediated ubiquitination of p53 are reported, and E 6-AP appears to have ubiquitin-protein ligase activity in the absence of E6.
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The Mutational Landscape of Head and Neck Squamous Cell Carcinoma
Nicolas Stransky,Ann Marie Egloff,Aaron D. Tward,Aaron D. Tward,Aaron D. Tward,Aleksandar Kostic,Aleksandar Kostic,Kristian Cibulskis,Andrey Sivachenko,Gregory Kryukov,Gregory Kryukov,Michael S. Lawrence,Carrie Sougnez,Aaron McKenna,Erica Shefler,Alex H. Ramos,Petar Stojanov,Scott L. Carter,Douglas Voet,Maria L. Cortes,Daniel Auclair,Michael F. Berger,Gordon Saksena,Candace Guiducci,Robert C. Onofrio,Melissa Parkin,Marjorie Romkes,Joel L. Weissfeld,Raja R. Seethala,Lin Wang,Claudia Rangel-Escareño,Juan Carlos Fernández-López,Alfredo Hidalgo-Miranda,Jorge Melendez-Zajgla,Wendy Winckler,Kristin Ardlie,Stacey Gabriel,Matthew Meyerson,Eric S. Lander,Eric S. Lander,Eric S. Lander,Gad Getz,Todd R. Golub,Levi A. Garraway,Jennifer R. Grandis +44 more
TL;DR: In this article, the authors analyzed whole-exome sequencing data from 74 tumor-normal pairs and found that at least 30% of cases harbored mutations in genes that regulate squamous differentiation (for example, NOTCH1, IRF6, and TP63), implicating its dysregulation as a major driver of HNSCC carcinogenesis.