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Lookup NU author(s): Dr Gabriele Saretzki, Professor Thomas von Zglinicki
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It has been repeatedly suspected that telomere shortening might be one possible trigger of the p53-dependent cell cycle arrest, although the mechanism of this arrest remained unclear. Telomeres in human cells under mild oxidative stress accumulate single-strand damage faster than interstitial repetitive sequences. In MRC-5 ®bro-blasts and U87 glioblastoma cells, which both express wild-type p53, oxidative stress-mediated production of single-strand damage in telomeres is concomitant to the accumulation of p53 and p21 and to cell cycle arrest. This response can be modeled by treatment of cells with short single stranded telomeric G-rich DNA fragments. The arrest is transient in U87 cells. Recovery from it is accompanied by up-regulation of telomerase activity and elongation of telomeres. Overexpression of mutated p53 is sufficient to reverse the phenotype of inhibition as well as the delayed activation of telomerase. These data suggest that the production of G-rich single stranded fragments during the course of telomere shortening is sufficient to trigger a p53 dependent cell cycle arrest.
Author(s): Saretzki G, Sitte N, Merkel U, Wurm RE, von Zglinicki T
Publication type: Article
Publication status: Published
Journal: Oncogene
Year: 1999
Volume: 18
Issue: 37
Pages: 5148-5158
Print publication date: 01/01/1999
ISSN (print): 0950-9232
ISSN (electronic): 1476-5594
Publisher: Nature Publishing Group
URL: http://dx.doi.org/10.1038/sj.onc.1202898
DOI: 10.1038/sj.onc.1202898
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