Nucleic Acids Research Advance Access originally published online on October 2, 2007
Nucleic Acids Research 2007 35(22):7466-7474; doi:10.1093/nar/gkm756
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Nucleic Acids Research, 2007, Vol. 35, No. 22 7466-7474
© 2007 The Author(s)
This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/2.0/uk/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.
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Changes in DNA repair during aging
Department of Biology, University of Rochester, Rochester, NY 14627, USA
*To whom correspondence should be addressed. Tel: +1 585 275 7740; Fax: +1 585 275 2070; Email: vgorbuno{at}mail.rochester.edu
Received July 2, 2007. Revised September 10, 2007. Accepted September 10, 2007.
DNA is a precious molecule. It encodes vital information about cellular content and function. There are only two copies of each chromosome in the cell, and once the sequence is lost no replacement is possible. The irreplaceable nature of the DNA sets it apart from other cellular molecules, and makes it a critical target for age-related deterioration. To prevent DNA damage cells have evolved elaborate DNA repair machinery. Paradoxically, DNA repair can itself be subject to age-related changes and deterioration. In this review we will discuss the changes in efficiency of mismatch repair (MMR), base excision repair (BER), nucleotide excision repair (NER) and double-strand break (DSB) repair systems during aging, and potential changes in DSB repair pathway usage that occur with age. Mutations in DNA repair genes and premature aging phenotypes they cause have been reviewed extensively elsewhere, therefore the focus of this review is on the comparison of DNA repair mechanisms in young versus old.
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