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Free Radical Biology and Medicine, ISSN 0891-5849, 11/2017, Volume 112, p. 161
To access, purchase, authenticate, or subscribe to the full-text of this article, please visit this link: http://dx.doi.org/10.1016/j.freeradbiomed.2017.10.247 
Niacinamide | Lactates | Glucose metabolism | Lysine
Journal Article
Free Radical Biology and Medicine, ISSN 0891-5849, 11/2017, Volume 112, pp. 161 - 161
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Journal of Biological Chemistry, ISSN 0021-9258, 01/2012, Volume 287, Issue 5, pp. 3573 - 3580
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Journal of Biological Chemistry, ISSN 0021-9258, 12/2015, Volume 290, Issue 51, p. 30267
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Nature, ISSN 0028-0836, 11/2014, Volume 515, Issue 7527, pp. 431 - 435
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British Journal of Pharmacology, ISSN 0007-1188, 04/2014, Volume 171, Issue 8, pp. 2091 - 2098
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Journal Article
FREE RADICAL BIOLOGY AND MEDICINE, ISSN 0891-5849, 11/2017, Volume 112, pp. 161 - 161
Conference Proceeding
Biochimica et Biophysica Acta - Molecular Cell Research, ISSN 0167-4889, 07/2011, Volume 1813, Issue 7, pp. 1309 - 1315
The mitochondrial ATP-sensitive potassium channel (mK ) is important in the protective mechanism of ischemic preconditioning (IPC). The channel is reportedly... 
channel | Redox | Ischemia | Preconditioning | Nitric oxide
Journal Article
BBA - Molecular Cell Research, ISSN 0167-4889, 07/2011, Volume 1813, Issue 7, p. 1309
The mitochondrial ATP-sensitive potassium channel (mK.sub.ATP) is important in the protective mechanism of ischemic preconditioning (IPC). The channel is... 
Laws, regulations and rules | Analysis | Nitric oxide | Mitochondrial DNA
Journal Article
Proceedings of the National Academy of Sciences of the United States of America, ISSN 0027-8424, 6/2009, Volume 106, Issue 26, pp. 10764 - 10769
Nitric oxide $(NO^ \bullet )$ competitively inhibits oxygen consumption by mitochondria at cytochrome c oxidase and 5-nitrosates thiol proteins. We developed... 
Oxidases | Electrodes | Mitochondria | Thiols | Cytochromes | Oxides | Oxygen consumption | Hypoxia | Respiration | Reperfusion injury | S-nitrosation | Nitric oxide | OXYGEN | nitric oxide | VIVO | COMPLEX-I | MULTIDISCIPLINARY SCIENCES | NITRIC-OXIDE | PROTEINS | CARDIOPROTECTION | Mitochondria, Heart - metabolism | Humans | Male | Membrane Potential, Mitochondrial - drug effects | S-Nitrosothiols - metabolism | Electron Transport Complex I - metabolism | Myoblasts - drug effects | Myoblasts - metabolism | Sulfhydryl Compounds - metabolism | Aorta, Thoracic - physiology | Mass Spectrometry | Myoblasts - cytology | Aorta, Thoracic - drug effects | Reperfusion Injury - metabolism | Heart - physiopathology | Cell Line | S-Nitrosothiols - pharmacology | S-Nitrosothiols - chemical synthesis | Mice, Inbred C57BL | Rats | Mitochondria - metabolism | Rats, Sprague-Dawley | Nitric Oxide - secretion | Animals | Reperfusion Injury - prevention & control | Mitochondria, Heart - physiology | Oxygen Consumption - drug effects | Nitrosation - drug effects | Reperfusion Injury - physiopathology | Heart - drug effects | Mice | HeLa Cells | Vasodilation - drug effects | In Vitro Techniques | Mitochondria - physiology | Prevention | Physiological aspects | Properties | Proteins | Oxygen | Membranes | Ischemia | Index Medicus | Biological Sciences
Journal Article
Biochimica et Biophysica Acta (BBA) - Bioenergetics, ISSN 0005-2728, 07/2010, Volume 1797, p. 81
Journal Article
American Journal of Physiology - Heart and Circulatory Physiology, ISSN 0363-6135, 10/2011, Volume 301, Issue 4, pp. 1506 - 1512
Overexpression studies have revealed a role for silent information regulator of transcription 1 (SIRT1) lysine deacetylase in cardioprotection against... 
Myocardial infarction | Nicotinamide adenine dinucleotide | Ischemic preconditioning | Silent information regulator of transcription | Lysine deacetylation | RESVERATROL | ACTIVATION | CARDIAC & CARDIOVASCULAR SYSTEMS | PHYSIOLOGY | NITRIC-OXIDE SYNTHASE | myocardial infarction | CARDIAC MYOCYTES | ischemic preconditioning | lysine deacetylation | AUTOPHAGY | FOXO TRANSCRIPTION FACTORS | CELL-SURVIVAL | SIRT1 DEACETYLASE | nicotinamide adenine dinucleotide | HEART | silent information regulator of transcription | PERIPHERAL VASCULAR DISEASE | ISCHEMIA/REPERFUSION | Animals, Genetically Modified | Heart - physiology | Mice, Inbred C57BL | Signal Transduction - genetics | Sirtuin 1 - antagonists & inhibitors | Sirtuin 1 - genetics | Blotting, Western | Myocardial Reperfusion Injury - physiopathology | Mice, Knockout | Animals | Forkhead Transcription Factors - metabolism | Ischemic Preconditioning, Myocardial | Sirtuin 1 - physiology | Cytosol - metabolism | Signal Transduction - physiology | Forkhead Box Protein O1 | Lysine - metabolism | Mice | Acetylation | In Vitro Techniques | Myocardial Reperfusion Injury - prevention & control | NAD - metabolism | Superoxide Dismutase - metabolism | Prevention | Physiological aspects | Research | Genetic transcription | Lysine | Reperfusion injury | Amino acids | Phosphorylation | Pharmacology | Ischemia | Gene expression | Rodents | Index Medicus | Signaling and Stress Response
Journal Article
Journal Article
PLoS ONE, ISSN 1932-6203, 05/2016, Volume 11, Issue 5, pp. e0155709 - e0155709
Pathogenic factors associated with aging, such as oxidative stress and hormone depletion converge on mitochondria and impair their function via opening of the... 
MITOCHONDRIAL PERMEABILITY TRANSITION | OXIDATIVE STRESS | OSTEOBLAST DIFFERENTIATION | MULTIDISCIPLINARY SCIENCES | PORE | DISEASE | INVOLVEMENT | CELL-DEATH | REVEALS | Bone and Bones - pathology | Age Factors | Cyclophilins - deficiency | Male | X-Ray Microtomography | Osteoporosis - metabolism | Bone Resorption - genetics | Bone and Bones - diagnostic imaging | Bone and Bones - metabolism | Osteoporosis - diagnostic imaging | Bone Resorption - metabolism | Osteoporosis - genetics | Disease Resistance - genetics | Disease Models, Animal | Genetic Predisposition to Disease | Bone Density | Metabolome | Mitochondria - metabolism | Metabolomics - methods | Osteoclasts - metabolism | Mice, Knockout | Biomechanical Phenomena | Phenotype | Animals | Osteoporosis - pathology | Mice | Osteoporosis | Care and treatment | Research | Cyclophilin | Analysis | Mitochondrial membranes | Brain | Oxidative stress | Metabolomics | Phosphorylation | Mitochondrial permeability transition pore | Oxidative metabolism | Impairment | Membrane permeability | Osteocytes | Mitochondrial DNA | Nucleotides | Mitochondria | Bone growth | NADH | Clonal deletion | Rodents | Deletion | Aging | Biocompatibility | Bone loss | Age | Cardiac muscle | Muscles | Permeability | Dentistry | Metabolism | Breeding of animals | Electron microscopy | Medicine | NAD | Biomechanics | Pathology | Bone mass | Stem cells | Nicotinamide adenine dinucleotide | Glycolysis | Bone | Anesthesiology | MPTP | Laboratory animals | Alzheimers disease | Osteogenesis | Apoptosis | Index Medicus
Journal Article
FASEB Journal, ISSN 0892-6638, 11/2018, Volume 32, Issue 11, pp. 6135 - 6149
Journal Article