| pubmed-article:17913742 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:17913742 | lifeskim:mentions | umls-concept:C0001811 | lld:lifeskim |
| pubmed-article:17913742 | lifeskim:mentions | umls-concept:C0012899 | lld:lifeskim |
| pubmed-article:17913742 | lifeskim:mentions | umls-concept:C0392747 | lld:lifeskim |
| pubmed-article:17913742 | lifeskim:mentions | umls-concept:C0443172 | lld:lifeskim |
| pubmed-article:17913742 | pubmed:issue | 22 | lld:pubmed |
| pubmed-article:17913742 | pubmed:dateCreated | 2008-1-4 | lld:pubmed |
| pubmed-article:17913742 | pubmed:abstractText | 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. | lld:pubmed |
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