Journal article
Acetylation of MnSOD directs enzymatic activity responding to cellular nutrient status or oxidative stress
Aging (Albany, NY.), Vol.3(2), pp.102-107
2011
DOI: 10.18632/aging.100291
PMCID: PMC3082006
PMID: 21386137
Abstract
A fundamental observation in biology is that mitochondrial function, as measured by increased reactive oxygen species (ROS), changes significantly with age, suggesting a potential mechanistic link between the cellular processes governing longevity and mitochondrial metabolism homeostasis. In addition, it is well established that altered ROS levels are observed in multiple age-related illnesses including carcinogenesis, neurodegenerative, fatty liver, insulin resistance, and cardiac disease, to name just a few. Manganese superoxide dismutase (MnSOD) is the primary mitochondrial ROS scavenging enzyme that converts superoxide to hydrogen peroxide, which is subsequently converted to water by catalase and other peroxidases. It has recently been shown that MnSOD enzymatic activity is regulated by the reversible acetylation of specific, evolutionarily conserved lysine(s) in the protein. These results, suggest for the first time, that the mitochondria contain bidirectional post-translational signaling networks, similar to that observed in the cytoplasm and nucleus, and that changes in lysine acetylation alter MnSOD enzymatic activity. In addition, these new results demonstrate that the mitochondrial anti-aging or fidelity / sensing protein, SIRT3, responds to changes in mitochondrial nutrient and/or redox status to alter the enzymatic activity of specific downstream targets, including MnSOD that adjusts and/or maintains ROS levels as well as metabolic homeostatic poise.
Details
- Title: Subtitle
- Acetylation of MnSOD directs enzymatic activity responding to cellular nutrient status or oxidative stress
- Creators
- Ozkan Ozden - Departments of Cancer Biology, Pediatrics, and Radiation Oncology, Vanderbilt University Medical Center, Nashville, TN 37232, USASeong-Hoon Park - Departments of Cancer Biology, Pediatrics, and Radiation Oncology, Vanderbilt University Medical Center, Nashville, TN 37232, USAHyun-Seok Kim - Departments of Cancer Biology, Pediatrics, and Radiation Oncology, Vanderbilt University Medical Center, Nashville, TN 37232, USAHaiyan Jiang - Departments of Cancer Biology, Pediatrics, and Radiation Oncology, Vanderbilt University Medical Center, Nashville, TN 37232, USAMitchell C Coleman - Free Radical and Radiation Biology Program, Department of Radiation Oncology, Holden Comprehensive Cancer Center, The University of Iowa, Iowa City, IA 52242, USADouglas R Spitz - Free Radical and Radiation Biology Program, Department of Radiation Oncology, Holden Comprehensive Cancer Center, The University of Iowa, Iowa City, IA 52242, USADavid Gius - Departments of Cancer Biology, Pediatrics, and Radiation Oncology, Vanderbilt University Medical Center, Nashville, TN 37232, USA
- Resource Type
- Journal article
- Publication Details
- Aging (Albany, NY.), Vol.3(2), pp.102-107
- DOI
- 10.18632/aging.100291
- PMID
- 21386137
- PMCID
- PMC3082006
- NLM abbreviation
- Aging (Albany NY)
- ISSN
- 1945-4589
- eISSN
- 1945-4589
- Publisher
- Impact Journals LLC
- Language
- English
- Date published
- 2011
- Academic Unit
- Pathology; Orthopedics and Rehabilitation; Radiation Oncology
- Record Identifier
- 9984040380602771
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