ReviewMethods (San Diego, Calif.)2010
Mitochondrial base excision repair assays.
Review in Methods (San Diego, Calif.), 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
23 citing papers in PubMed.
- Simultaneous quantification of mitochondrial DNA damage and copy number in circulating blood: a sensitive approach to systemic oxidative stress.BioMed research international · 2013Trial
- Oxidative Stress in DNA Damage and Neurodegenerative Diseases: Unveiling The Mechanisms and Therapeutic Opportunities.Cell biochemistry and biophysics · 2025Review
- Dysregulation of DNA repair genes in Fuchs endothelial corneal dystrophy.Experimental eye research · 2023Article
- Dynamic features of human mitochondrial DNA maintenance and transcription.Frontiers in cell and developmental biology · 2022Review
- Barth syndrome cardiomyopathy: targeting the mitochondria with elamipretide.Heart failure reviews · 2021Review
- Arginine methylation of APE1 promotes its mitochondrial translocation to protect cells from oxidative damage.Free radical biology & medicine · 2020Article
- Interaction between RECQL4 and OGG1 promotes repair of oxidative base lesion 8-oxoG and is regulated by SIRT1 deacetylase.Nucleic acids research · 2020Article
- Targeting the Mitochondria in Heart Failure: A Translational Perspective.JACC. Basic to translational science · 2020Review
- Maternal transmission of mitochondrial diseases.Genetics and molecular biology · 2020Article
- Newly Revised Quantitative PCR-Based Assay for Mitochondrial and Nuclear DNA Damage.Current protocols in toxicology · 2018Article
- Formation and repair of oxidatively generated damage in cellular DNA.Free radical biology & medicine · 2017Review
- Lack of XPC leads to a shift between respiratory complexes I and II but sensitizes cells to mitochondrial stress.Scientific reports · 2017Article
- Bcl2 inhibition of mitochondrial DNA repair.BMC cancer · 2015Article
- Slow mitochondrial repair of 5'-AMP renders mtDNA susceptible to damage in APTX deficient cells.Scientific reports · 2015Article
- Distinct Phenotypes Caused by Mutation of MSH2 in Trypanosome Insect and Mammalian Life Cycle Forms Are Associated with Parasite Adaptation to Oxidative Stress.PLoS neglected tropical diseases · 2015Article
- Mitochondrial DNA damage as a peripheral biomarker for mitochondrial toxin exposure in rats.Toxicological sciences : an official journal of the Society of Toxicology · 2014Article
- Mitochondria, energetics, epigenetics, and cellular responses to stress.Environmental health perspectives · 2014Review
- Mitochondrial DNA damage: molecular marker of vulnerable nigral neurons in Parkinson's disease.Neurobiology of disease · 2014Article
- Oxidative damage to macromolecules in human Parkinson disease and the rotenone model.Free radical biology & medicine · 2013Review
- Endonuclease VIII-like 1 (NEIL1) promotes short-term spatial memory retention and protects from ischemic stroke-induced brain dysfunction and death in mice.Proceedings of the National Academy of Sciences of the United States of America · 2012Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors.
Funding
Abstract
The main source of mitochondrial DNA (mtDNA) damage is reactive oxygen species (ROS) generated during normal cellular metabolism. The main mtDNA lesions generated by ROS are base modifications, such as the ubiquitous 8-oxoguanine (8-oxoG) lesion; however, base loss and strand breaks may also occur. Many human diseases are associated with mtDNA mutations and thus maintaining mtDNA integrity is critical. All of these lesions are repaired primarily by the base excision repair (BER) pathway. It is now known that mammalian mitochondria have BER, which, similarly to nuclear BER, is catalyzed by DNA glycosylases, AP endonuclease, DNA polymerase (POLgamma in mitochondria) and DNA ligase. This article outlines procedures for measuring oxidative damage formation and BER in mitochondria, including isolation of mitochondria from tissues and cells, protocols for measuring BER enzyme activities, gene-specific repair assays, chromatographic techniques as well as current optimizations for detecting 8-oxoG lesions in cells by immunofluorescence. Throughout the assay descriptions we will include methodological considerations that may help optimize the assays in terms of resolution and repeatability.
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What OpenQuestion holds
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.