Journal Article

Poly(ADP-ribose) polymerase activity is not affected in ataxia telangiectasia cells and knockout mice

Françoise Dantzer, Josiane Ménissier-de Murcia, Carrolee Barlow, Anthony Wynshaw-Boris and Gilbert de Murcia

in Carcinogenesis

Volume 20, issue 1, pages 177-180
Published in print January 1999 | ISSN: 0143-3334
Published online January 1999 | e-ISSN: 1460-2180 | DOI: http://dx.doi.org/10.1093/carcin/20.1.177
Poly(ADP-ribose) polymerase activity is not affected in ataxia telangiectasia cells and knockout mice

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Poly(ADP-ribose) polymerase (PARP) is a constitutive factor of the DNA damage surveillance network in dividing cells. Based on its capacity to bind to DNA strand breaks, PARP plays a regulatory role in their resolution in vivo. ATM belongs to a large family of proteins involved in cell cycle progression and checkpoints in response to DNA damage. Both proteins may act as sensors of DNA damage to induce multiple signalling pathways leading to activation of cell cycle checkpoints and DNA repair. To determine a possible relationship between PARP and ATM, we examined the PARP response in an ATM-null background. We demonstrated that ATM deficiency does not affect PARP activity in human cell lines or Atm-deficient mouse tissues, nor does it alter PARP activity induced by oxidative damage or γ-irradiation. Our results support a model in which PARP and ATM could be involved in distinct pathways, both effectors transducing the damage signal to cell cycle regulators.

Keywords: AT, ataxia telangiectasia; BSA, bovine serum albumin; DSB, double-strand breaks; PARP, poly(ADP-ribose) polymerase; PBS, phosphate-buffered saline; SSB, single-strand breaks.

Journal Article.  2747 words.  Illustrated.

Subjects: Clinical Cytogenetics and Molecular Genetics

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