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Title: Papillomavirus E6 proteins

Abstract

The papillomaviruses are small DNA viruses that encode approximately eight genes, and require the host cell DNA replication machinery for their viral DNA replication. Thus papillomaviruses have evolved strategies to induce host cell DNA synthesis balanced with strategies to protect the cell from unscheduled replication. While the papillomavirus E1 and E2 genes are directly involved in viral replication by binding to and unwinding the origin of replication, the E6 and E7 proteins have auxillary functions that promote proliferation. As a consequence of disrupting the normal checkpoints that regulate cell cycle entry and progression, the E6 and E7 proteins play a key role in the oncogenic properties of human papillomaviruses with a high risk of causing anogenital cancers (HR HPVs). As a consequence, E6 and E7 of HR HPVs are invariably expressed in cervical cancers. This article will focus on the E6 protein and its numerous activities including inactivating p53, blocking apoptosis, activating telomerase, disrupting cell adhesion, polarity and epithelial differentiation, altering transcription and reducing immune recognition.

Authors:
 [1];  [1]
  1. Division of Human Biology, Fred Hutchinson Cancer Research Center, 1100 Fairview Avenue North, C1-015, Box 19024, Seattle, WA 98109-1024 (United States)
Publication Date:
OSTI Identifier:
21182804
Resource Type:
Journal Article
Journal Name:
Virology
Additional Journal Information:
Journal Volume: 384; Journal Issue: 2; Other Information: DOI: 10.1016/j.virol.2008.11.017; PII: S0042-6822(08)00725-3; Copyright (c) 2008 Elsevier Science B.V., Amsterdam, The Netherlands, All rights reserved; Country of input: International Atomic Energy Agency (IAEA); Journal ID: ISSN 0042-6822
Country of Publication:
United States
Language:
English
Subject:
60 APPLIED LIFE SCIENCES; ADHESION; APOPTOSIS; CELL CYCLE; CELL PROLIFERATION; DNA; DNA REPLICATION; HOST; NEOPLASMS; ONCOGENES; PROTEINS; SYNTHESIS; TRANSCRIPTION; VIRUSES

Citation Formats

Howie, Heather L, Katzenellenbogen, Rachel A, Department of Pediatrics, University of Washington, Seattle, Washington, and Galloway, Denise A. Papillomavirus E6 proteins. United States: N. p., 2009. Web. doi:10.1016/j.virol.2008.11.017.
Howie, Heather L, Katzenellenbogen, Rachel A, Department of Pediatrics, University of Washington, Seattle, Washington, & Galloway, Denise A. Papillomavirus E6 proteins. United States. https://doi.org/10.1016/j.virol.2008.11.017
Howie, Heather L, Katzenellenbogen, Rachel A, Department of Pediatrics, University of Washington, Seattle, Washington, and Galloway, Denise A. 2009. "Papillomavirus E6 proteins". United States. https://doi.org/10.1016/j.virol.2008.11.017.
@article{osti_21182804,
title = {Papillomavirus E6 proteins},
author = {Howie, Heather L and Katzenellenbogen, Rachel A and Department of Pediatrics, University of Washington, Seattle, Washington and Galloway, Denise A.},
abstractNote = {The papillomaviruses are small DNA viruses that encode approximately eight genes, and require the host cell DNA replication machinery for their viral DNA replication. Thus papillomaviruses have evolved strategies to induce host cell DNA synthesis balanced with strategies to protect the cell from unscheduled replication. While the papillomavirus E1 and E2 genes are directly involved in viral replication by binding to and unwinding the origin of replication, the E6 and E7 proteins have auxillary functions that promote proliferation. As a consequence of disrupting the normal checkpoints that regulate cell cycle entry and progression, the E6 and E7 proteins play a key role in the oncogenic properties of human papillomaviruses with a high risk of causing anogenital cancers (HR HPVs). As a consequence, E6 and E7 of HR HPVs are invariably expressed in cervical cancers. This article will focus on the E6 protein and its numerous activities including inactivating p53, blocking apoptosis, activating telomerase, disrupting cell adhesion, polarity and epithelial differentiation, altering transcription and reducing immune recognition.},
doi = {10.1016/j.virol.2008.11.017},
url = {https://www.osti.gov/biblio/21182804}, journal = {Virology},
issn = {0042-6822},
number = 2,
volume = 384,
place = {United States},
year = {Fri Feb 20 00:00:00 EST 2009},
month = {Fri Feb 20 00:00:00 EST 2009}
}