ArticleOncogene2012
Manganese superoxide dismutase is a mitochondrial fidelity protein that protects Polγ against UV-induced inactivation.
Article in Oncogene, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 52 citations in OpenAlex.
- Mitochondrial DNA replication is regulated by endoplasmic reticulum-mitochondrial contact sites, the mitochondrial calcium uniporter, and manganese.Nucleic acids research · 2026Article
- DNA Polymerase Gamma Acetylation Governs Mitochondrial Homeostasis and Vascular Cell Senescence.International journal of biological sciences · 2026Article
- Expression, Purification, and Anti-UV Irradiation Effect of RsSOD on HCE-T Human Corneal Epithelial Cells.Genes · 2024Article
- Mitochondrial Genome-Encoded Long Noncoding RNA and Mitochondrial Stability in Diabetic Retinopathy.Diabetes · 2023Article
- DNA Polymerase Gamma Recovers Mitochondrial Function and Inhibits Vascular Calcification by Interacted with p53.International journal of biological sciences · 2022Article
- Suppression of Fusarium Wilt Caused byJournal of microbiology and biotechnology · 2021Article
- Mitochondrial DNA-depleter mouse as a model to study human pigmentary skin disorders.Pigment cell & melanoma research · 2021Article
- Mitochondrial Superoxide Dismutase: What the Established, the Intriguing, and the Novel Reveal About a Key Cellular Redox Switch.Antioxidants & redox signaling · 2020Review
- UVB-induced inactivation of manganese-containing superoxide dismutase promotes mitophagy via ROS-mediated mTORC2 pathway activation.The Journal of biological chemistry · 2019Article
- GABA, γ-Aminobutyric Acid, Protects Against Severe Liver Injury.The Journal of surgical research · 2019Article
- Mn Porphyrin-Based Redox-Active Drugs: Differential Effects as Cancer Therapeutics and Protectors of Normal Tissue Against Oxidative Injury.Antioxidants & redox signaling · 2018Review
- Post-Irradiation Treatment with a Superoxide Dismutase Mimic, MnTnHex-2-PyPAntioxidants (Basel, Switzerland) · 2018Article
- Carnosic Acid Suppresses the HMolecular neurobiology · 2018Article
- Role of p53, Mitochondrial DNA Deletions, and Paternal Age in Autism: A Case-Control Study.Pediatrics · 2016Article
- Mitochondrial translocation of p53 modulates neuronal fate by preventing differentiation-induced mitochondrial stress.Antioxidants & redox signaling · 2014Article
- p53 and mitochondrial function in neurons.Biochimica et biophysica acta · 2014Review
- Manganese superoxide dismutase-mediated inside-out signaling in HaCaT human keratinocytes and SKH-1 mouse skin.Antioxidants & redox signaling · 2014Article
- Antioxidant gene therapy against neuronal cell death.Pharmacology & therapeutics · 2014Review
- The use of the Cre/loxP system to study oxidative stress in tissue-specific manganese superoxide dismutase knockout models.Antioxidants & redox signaling · 2014Review
- Tauroursodeoxycholic acid increases neural stem cell pool and neuronal conversion by regulating mitochondria-cell cycle retrograde signaling.Cell cycle (Georgetown, Tex.) · 2014Article
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
Abstract
Manganese superoxide dismutase is a nuclear encoded primary antioxidant enzyme localized exclusively in the mitochondrial matrix. Genotoxic agents, such as ultraviolet (UV) radiation, generates oxidative stress and cause mitochondrial DNA (mtDNA) damage. The mtDNA polymerase (Polγ), a major constituent of nucleoids, is responsible for the replication and repair of the mitochondrial genome. Recent studies suggest that the mitochondria contain fidelity proteins and MnSOD constitutes an integral part of the nucleoid complex. However, it is not known whether or how MnSOD participates in the mitochondrial repair processes. Using skin tissue from C57BL/6 mice exposed to UVB radiation, we demonstrate that MnSOD has a critical role in preventing mtDNA damage by protecting the function of Polγ. Quantitative-PCR analysis shows an increase in mtDNA damage after UVB exposure. Immunofluorescence and immunoblotting studies demonstrate p53 translocation to the mitochondria and interaction with Polγ after UVB exposure. The mtDNA immunoprecipitation assay with Polγ and p53 antibodies in p53(+/+) and p53(-/-) mice demonstrates an interaction between MnSOD, p53 and Polγ. The results suggest that these proteins form a complex for the repair of UVB-associated mtDNA damage. The data also demonstrate that UVB exposure injures the mtDNA D-loop in a p53-dependent manner. Using MnSOD-deficient mice we demonstrate that UVB-induced mtDNA damage is MnSOD dependent. Exposure to UVB results in nitration and inactivation of Polγ, which is prevented by addition of the MnSOD mimetic Mn(III)TE-2-PyP(5+). These results demonstrate for the first time that MnSOD is a fidelity protein that maintains the activity of Polγ by preventing UVB-induced nitration and inactivation of Polγ. The data also demonstrate that MnSOD has a role along with p53 to prevent mtDNA damage.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.