DNA repair and PARP in aging.
Half a century ago, when the free radical theory of aging was first proposed, the damaging effects of reactive oxygen species (ROS) were in the focus of attention and considered the single most important determinant of aging. Two decades later, however, the disposable soma theory of aging redirected the attention to the potential impact of cellular maintenance and repair pathways that are both genetically and environmentally determined and are counteracting the damaging effects of ROS. In the present paper, recent experimental data linking DNA repair pathways with the aging process are summarised. Special attention is paid to poly(ADP-ribosyl)ation, a DNA-damage driven posttranslational modification of proteins.
Bürkle
Alexander
A
Molecular Toxicology Group, University of Konstanz, Box X911, D-78457, Konstanz, Germany. alexander.buerkle@uni-konstanz.de
D000375:Aging / Q000502:physiology*; D000818:Animals; D034961:Antigens, Nuclear / Q000502:physiology; D003057:Cockayne Syndrome / Q000503:physiopathology; D053843:DNA Mismatch Repair; D004260:DNA Repair / Q000502:physiology*; D004268:DNA-Binding Proteins / Q000502:physiology; D006801:Humans; D000072200:Ku Autoantigen; D011064:Poly Adenosine Diphosphate Ribose / Q000378:metabolism; D011065:Poly(ADP-ribose) Polymerases / Q000502:physiology*
D034961:Antigens, Nuclear; D004268:DNA-Binding Proteins; D011064:Poly Adenosine Diphosphate Ribose; D011065:Poly(ADP-ribose) Polymerases; C000606509:Xrcc6 protein, human; D000072200:Ku Autoantigen