Доступ предоставлен для: Guest
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/CritRevEukarGeneExpr.v21.i4.30
pages 323-336

Replication of Damaged Genomes

Alden C. Klarer
Department of Biochemistry and Molecular Biology, University of Louisville; James Graham Brown Cancer Center, University of Louisville
W. Glenn McGregor
University of Louisville

Краткое описание

Cellular DNA is continuously assaulted by chemical and physical agents that arise from both endogenous metabolic processes as well as exogenous insults. Commonly encountered environmental agents include polyaromatic hydrocarbons, polycyclic aromatic amines, the ultraviolet component of sunlight, and ionizing radiation, among many others. Although the kinds of damages and the mechanisms involved in their interaction with DNA vary widely, genotoxic agents alter the structure of DNA in ways that may result in permanent alterations in the DNA sequence or in cell death. To avoid these consequences, cells have evolved countermeasures to reduce the biological consequences of DNA damage. These mechanisms are highly conserved and are present in all eukaryotic cells. In general, cellular responses include the detection of damage, signal transduction to halt cell cycle progression, and the recruitment of repair mechanisms that are tailored to the specific kind of damage. If replication-blocking damage remains when cells enter S-phase, then tolerance mechanisms in the form of complex recombination mechanisms or translesion DNA synthesis using accessory DNA polymerases exist. These mechanisms complete the replication of damaged genomes and suppress cytotoxicity, but at the potential cost of mutagenesis and genomic instability. This review focuses on error-prone mechanisms, including a discussion of the Y-family of DNA polymerases, current concepts of DNA polymerase switching mechanisms, and their relevance to cancer and cancer prevention.


Articles with similar content:

Role of c-MET in Upper Aerodigestive Malignancies — From Biology to Novel Therapies
Journal of Environmental Pathology, Toxicology and Oncology, Vol.24, 2005, issue 3
Radha Uppalapati, Tanguy Y. Seiwert, Sascha Dietrich, Patrick C. Ma
Transcription from the Perspective of the DNA: Twists and Bumps in the Road
Critical Reviews™ in Eukaryotic Gene Expression, Vol.13, 2003, issue 1
Jeffrey D. Parvin, Neelima Mondal
Genome Instability in the Context of Chromatin Structure and Fragile Sites
Critical Reviews™ in Eukaryotic Gene Expression, Vol.20, 2010, issue 3
Eva Bartova, Gabriela Galiova, Sona Legartova, Alzbeta Jugova, Lenka Stixova, Stanislav Kozubek
Retinoid Targets for the Treatment of Cancer
Critical Reviews™ in Eukaryotic Gene Expression, Vol.16, 2006, issue 3
Dianne Robert Soprano, Zivjena Buletic, Kenneth J. Soprano
Mammalian Cell DNA Replication
Critical Reviews™ in Eukaryotic Gene Expression, Vol.7, 1997, issue 1-2
Robert J. Hickey , Linda H. Malkas