Overcoming ATM Deficiency by Activating the NAD+/SIRT1 Axis

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Overcoming ATM Deficiency by Activating the NAD+/SIRT1 Axis Leonard Guarente Cell Metabolism Volume 24, Issue 4, Pages 526-528 (October 2016) DOI: 10.1016/j.cmet.2016.09.019 Copyright © 2016 Elsevier Inc. Terms and Conditions

Figure 1 Suppression of ATM−/− Phenotypes by NR ATM depletion results in inactivation of the Mre11-Rad50-Nbs1 (MRN) complex, Ku70, and DNA protein kinase (DNAPK), thereby causing persistent DNA damage, PARP activation, and NAD+ consumption. The resulting NAD+ deficiency then leads to SIRT1 inactivation, a defect in mitophagy, and mitochondrial dysfunction. NR restores mitochondrial function by reactivating SIRT1 and rescues DNA damage by activating Ku70 and DNAPK via SIRT1 and SIRT6. As a result, improved mitochondrial health and longer lifespan are provided to ATM−/− mice by NR. Cell Metabolism 2016 24, 526-528DOI: (10.1016/j.cmet.2016.09.019) Copyright © 2016 Elsevier Inc. Terms and Conditions