Additional file 1: Figure S1. of Exercise-induced mitochondrial p53 repairs mtDNA mutations in mutator mice

Autor: Adeel Safdar, Khrapko, Konstantin, Flynn, James, Saleem, Ayesha, Lisio, Michael, Johnston, Adam, Yevgenya Kratysberg, Samjoo, Imtiaz, Kitaoka, Yu, Ogborn, Daniel, Little, Jonathan, Raha, Sandeep, Parise, Gianni, Akhtar, Mahmood, Hettinga, Bart, Rowe, Glenn, Zoltan Arany, Prolla, Tomas, Tarnopolsky, Mark
Rok vydání: 2016
DOI: 10.6084/m9.figshare.c.3636737_d1.v1
Popis: Endurance exercise confers complete phenotype protection, suppresses early mortality, mitigates mitochondrial ROS-mediated oxidative damage, increases cellular antioxidant capacity, and 4 prevents cellular senescencmutator mice. Figure S2. Endurance exercise prevents dysregulated mitochondrial-induced apoptosis and reduces nuclear p53-mediated repression of PGC-1Îą and promotes mitochondrial biogenesis in mutator mice. Figure S3. Endurance exercise promotes systemic mitochondrial biogenesis in mtDNA mutator mice. Figure S4. Magnitude of mitochondrial ROS (physiological vs. pathological) regulates p53 subcellular localization. Figure S5. Pre-treatment with exogenous antioxidant preferentially shuttles p53 to mitochondria in response to stress. Figure S6. Endurance exercise-mediated attenuation of sarcopenia, increase in endurance capacity, skeletal muscle mitochondrial biogenesis, and repair of muscle mtDNA mutations is p53 dependent. Table S1. WT, PolG-SED, and PolG-END Skeletal Muscle Microarray IPA-GO Analysis. Table S2. Real-time PCR primer sequences. (PDF 1601Â kb)
Databáze: OpenAIRE