Apoptosis Induced by Persistent Single-strand Breaks in the Mitochondrial Genome: Critical Role of Exog (5’ Exo/endonuclease) in Their Repair
نویسندگان
چکیده
1 Department of Biochemistry & Molecular Biology, 2 Department of Microbiology & Immunology, University of Texas Medical Branch, 301 University Boulevard, Galveston, TX 77555-1079, USA, 3 Institute of Biochemistry, Faculty of Biology and Chemistry, Justus-LiebigUniversity, Heinrich-Buff-Ring 58, 35392 Giessen, Germany, 4 Department of Pharmacology and Chemical Biology, University of Pittsburgh Cancer Institute, 5117 Centre Avenue Pittsburgh, PA 15213-1863, USA Running title: Mitochondrial DNA Damage-Induced Apoptosis *Address correspondence to: Bartosz Szczesny, PhD, tel (409) 772-2174; fax (409) 747 8608, email: [email protected]
منابع مشابه
Apoptosis induced by persistent single-strand breaks in mitochondrial genome: critical role of EXOG (5'-EXO/endonuclease) in their repair.
Reactive oxygen species (ROS), continuously generated as by-products of respiration, inflict more damage on the mitochondrial (mt) than on the nuclear genome because of the nonchromatinized nature and proximity to the ROS source of the mitochondrial genome. Such damage, particularly single-strand breaks (SSBs) with 5'-blocking deoxyribose products generated directly or as repair intermediates f...
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The mitochondrial genome is highly susceptible to damage by reactive oxygen species (ROS) generated endogenously as a byproduct of respiration. ROS-induced DNA lesions, including oxidized bases, abasic (AP) sites, and oxidized AP sites, cause DNA strand breaks and are repaired via the base excision repair (BER) pathway in both the nucleus and mitochondria. Repair of damaged bases and AP sites i...
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Recently, a locus at the mitochondrial exo/endonuclease EXOG gene, which has been implicated in mitochondrial DNA repair, was associated with cardiac function. The function of EXOG in cardiomyocytes is still elusive. Here we investigated the role of EXOG in mitochondrial function and hypertrophy in cardiomyocytes. Depletion of EXOG in primary neonatal rat ventricular cardiomyocytes (NRVCs) indu...
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