@article{Burkle2004PolyA-52111,
  year={2004},
  doi={10.1016/j.exger.2004.07.010},
  title={Poly(ADP-ribosyl)ation and aging},
  number={11-12},
  volume={39},
  issn={0531-5565},
  journal={Experimental Gerontology},
  pages={1599--1601},
  author={Bürkle, Alexander and Beneke, Sascha and Muiras, Marie-Laure}
}

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    <dc:creator>Muiras, Marie-Laure</dc:creator>
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    <dcterms:title>Poly(ADP-ribosyl)ation and aging</dcterms:title>
    <dcterms:abstract xml:lang="eng">Poly(ADP-ribosyl)ation is a DNA strand break-driven post-translational modification of proteins catalyzed by poly(ADP-ribose) polymerase-1 (PARP-1), with NAD+ serving as substrate. Poly(ADP-ribosyl)ation is triggered by DNA strand breaks, is functionally associated with DNA repair pathways and is a survival factor for cells under low to moderate levels of genotoxic stress. We have previously described a positive correlation between poly(ADP-ribosyl)ation capacity of mononuclear blood cells with longevity of mammalian species. Our comparison of purified recombinant human and rat PARP-1 revealed that this correlation might be explained in part by evolutionary sequence divergence. We have also developed molecular genetic approaches to modulate the poly(ADP-ribosyl)ation status in living cells. Our results revealed that PARP-1 acts as a negative regulator of DNA damage-induced genomic instability, the latter being known as an important driving force for carcinogenesis. Our recent data obtained in transgenic mice with selective expression of a dominant negative version of PARP-1 in basal skin keratinocytes indicate that PARP-1 activity suppresses skin papilloma formation in a two-stage skin carcinogenesis protocol. It is tempting to speculate that increased poly(ADP-ribosyl)ation capacity in long-lived species might help retard the accumulation of DNA damage and of mutations and thus slow down the rate of aging and of carcinogenesis more efficiently as compared with short-lived animals.</dcterms:abstract>
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    <dc:contributor>Bürkle, Alexander</dc:contributor>
    <dc:creator>Beneke, Sascha</dc:creator>
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    <dc:contributor>Muiras, Marie-Laure</dc:contributor>
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