ARTD1 (PARP1) activation and NAD+ in DNA repair and cell death

Nicotinamide adenine dinucleotide, NAD+, is a small metabolite coenzyme that is essential for the progress of crucial cellular pathways including glycolysis, the tricarboxylic acid cycle (TCA) and mitochondrial respiration. These processes consume and produce both oxidative and reduced forms of NAD...

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Bibliographic Details
Published in:DNA repair 2014-11, Vol.23, p.27-32
Main Authors: Fouquerel, Elise, Sobol, Robert W.
Format: Article
Language:English
Subjects:
ADP(ribosyl)ation
Animals
Cell Death - genetics
DNA Damage
DNA Repair - physiology
Energy depletion
Enzyme Activation
Glycolysis
Humans
Metabolic defects
Metabolic Networks and Pathways
NAD
NAD - metabolism
Oxidation-Reduction
Poly (ADP-Ribose) Polymerase-1
Poly Adenosine Diphosphate Ribose - metabolism
Poly(ADP-ribose) Polymerases - metabolism
Sirtuins - metabolism
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Summary:Nicotinamide adenine dinucleotide, NAD+, is a small metabolite coenzyme that is essential for the progress of crucial cellular pathways including glycolysis, the tricarboxylic acid cycle (TCA) and mitochondrial respiration. These processes consume and produce both oxidative and reduced forms of NAD (NAD+ and NADH). NAD+ is also important for ADP(ribosyl)ation reactions mediated by the ADP-ribosyltransferase enzymes (ARTDs) or deacetylation reactions catalyzed by the sirtuins (SIRTs) which use NAD+ as a substrate. In this review, we highlight the significance of NAD+ catabolism in DNA repair and cell death through its utilization by ARTDs and SIRTs. We summarize the current findings on the involvement of ARTD1 activity in DNA repair and most specifically its involvement in the trigger of cell death mediated by ARTD1 activation and energy depletion. By sharing the same substrate, the activities of ARTDs and SIRTs are tightly linked, are dependent on each other and are thereby involved in the same cellular processes that play an important role in cancer biology, inflammatory diseases and ischaemia/reperfusion.
ISSN:1568-7864
1568-7856
DOI:10.1016/j.dnarep.2014.09.004