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Портал Begell Электронная Бибилиотека e-Книги Журналы Справочники и Сборники статей Коллекции
Critical Reviews™ in Eukaryotic Gene Expression
Импакт фактор: 1.841 5-летний Импакт фактор: 1.927 SJR: 0.649 SNIP: 0.516 CiteScore™: 1.96

ISSN Печать: 1045-4403
ISSN Онлайн: 2162-6502

Выпуски:
Том 29, 2019 Том 28, 2018 Том 27, 2017 Том 26, 2016 Том 25, 2015 Том 24, 2014 Том 23, 2013 Том 22, 2012 Том 21, 2011 Том 20, 2010 Том 19, 2009 Том 18, 2008 Том 17, 2007 Том 16, 2006 Том 15, 2005 Том 14, 2004 Том 13, 2003 Том 12, 2002 Том 11, 2001 Том 10, 2000 Том 9, 1999 Том 8, 1998 Том 7, 1997 Том 6, 1996 Том 5, 1995 Том 4, 1994

Critical Reviews™ in Eukaryotic Gene Expression

DOI: 10.1615/CritRevEukaryotGeneExpr.v14.i3.30
20 pages

Regulation of Cell Cycle Progression and Apoptosis by the Papillomavirus E6 Oncogene

Xueli Fan
Department of Medicine, University of Massachusetts Medical School, 364 Plantation Street, Worcester, MA 01605-2324
Jason J. Chen
Department of Medicine, University of Massachusetts Medical School, 364 Plantation Street, Worcester, MA 01605-2324

Краткое описание

Infection with human papillomaviruses (HPV) is strongly associated with the development of cervical cancer. The HPV E6 gene is essential for the oncogenic potential of HPV. E6 abrogates multiple cell cycle checkpoints and modulates apoptosis. Loss of cell cycle checkpoints contributes to genomic instability, a hallmark of cancer cells. Cancer cells also show reduced propensity for apoptotic cell death. Inactivation of the tumor suppressor p53 by E6 is an important mechanism by which E6 promotes cell growth. The molecular basis for apoptosis modulation by E6 is poorly understood. Although it is expected that inactivation of p53 by E6 should lead to a reduction in cellular apoptosis, numerous studies showed that E6 could in fact sensitize cells to apoptosis. In this article, we present an overview of observations and current understanding of the molecular basis for E6-induced cell proliferation and apoptosis.


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