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Lookup NU author(s): Barbara Keys,
Dr Gabriele Saretzki,
Professor Thomas von Zglinicki
Full text for this publication is not currently held within this repository. Alternative links are provided below where available.
Telomeres shorten in human somatic cells with each round of DNA replication, and this shortening is thought to ultimately trigger replicative senescence. Telomere shortening is caused partly by the inability of semiconservative DNA replication to copy a linear strand of DNA to its very end. Post-replicative processing of telomeric ends, producing single-stranded G-rich 3′ overhangs, has also been suggested to contribute to telomere shortening. This suggestion implies that a positive correlation should exist between the length of 3′ overhangs and the rate of telomere shortening. We confirmed shortening of overhangs as human lung (MRC5) and foreskin (BJ) fibroblasts approach senescence by measuring overhang length using in-gel hybridization. However, a large study of fibroblast strains from 21 donors maintained under conditions which lead to two orders of magnitude of variation in telomere shortening rate failed to show any correlation between telomere overhang length and shortening rate, suggesting that overhang length is neither a cause nor a correlate of telomere shortening. © Blackwell Publishing Ltd/Anatomical Society of Great Britain and Ireland 2004.
Author(s): Keys B, Serra V, Saretzki G, von Zglinicki T
Publication type: Article
Publication status: Published
Journal: Aging Cell
ISSN (print): 1474-9718
ISSN (electronic): 1474-9726
PubMed id: 15153178
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