ArticleDNA repair2014
Overexpression of DNA ligase III in mitochondria protects cells against oxidative stress and improves mitochondrial DNA base excision repair.
Article in DNA repair, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
What it found
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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.
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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.
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Who cites it
22 citing papers in PubMed, 43 citations in OpenAlex.
- Ligase 3 prevents oxidative strand break-induced mitochondrial DNA loss but is not essential for replicative circularization.Nucleic acids research · 2025Article
- Genomic stress in diseases stemming from defects in the second brain.Neurogastroenterology and motility · 2025Review
- Horizontal acquisition of a DNA ligase improves DNA damage tolerance in eukaryotes.Nature communications · 2023Article
- Without a pinch of salt: effect of low salinity on eggs and nauplii of the salmon louse (Lepeophtheirus salmonis).Parasitology research · 2023Article
- CircRNA Galntl6 sponges miR-335 to ameliorate stress-induced hypertension through upregulating Lig3 in rostral ventrolateral medulla.Redox biology · 2023Article
- Fueling genome maintenance: On the versatile roles of NADThe Journal of biological chemistry · 2022Review
- Dynamic features of human mitochondrial DNA maintenance and transcription.Frontiers in cell and developmental biology · 2022Review
- Myopathic mitochondrial DNA depletion syndrome associated with biallelic variants in LIG3.Brain : a journal of neurology · 2021Article
- DNA polymerase β outperforms DNA polymerase γ in key mitochondrial base excision repair activities.DNA repair · 2021Article
- The Similarities between Human Mitochondria and Bacteria in the Context of Structure, Genome, and Base Excision Repair System.Molecules (Basel, Switzerland) · 2020Review
- Mitophagy and DNA damage signaling in human aging.Mechanisms of ageing and development · 2020Review
- Altered DNA ligase activity in human disease.Mutagenesis · 2020Review
- Review
- Mitochondria in the signaling pathways that control longevity and health span.Ageing research reviews · 2019Review
- Diminished OPA1 expression and impaired mitochondrial morphology and homeostasis in Aprataxin-deficient cells.Nucleic acids research · 2019Article
- Structures of DNA-bound human ligase IV catalytic core reveal insights into substrate binding and catalysis.Nature communications · 2018Article
- DNA Polymerase Beta Participates in Mitochondrial DNA Repair.Molecular and cellular biology · 2017Article
- DNA Damage, DNA Repair, Aging, and Neurodegeneration.Cold Spring Harbor perspectives in medicine · 2015Review
- Human DNA ligase III bridges two DNA ends to promote specific intermolecular DNA end joining.Nucleic acids research · 2015Article
- Slow mitochondrial repair of 5'-AMP renders mtDNA susceptible to damage in APTX deficient cells.Scientific reports · 2015Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
Abstract
Base excision repair (BER) is the most prominent DNA repair pathway in human mitochondria. BER also results in a temporary generation of AP-sites, single-strand breaks and nucleotide gaps. Thus, incomplete BER can result in the generation of DNA repair intermediates that can disrupt mitochondrial DNA replication and transcription and generate mutations. We carried out BER analysis in highly purified mitochondrial extracts from human cell lines U2OS and HeLa, and mouse brain using a circular DNA substrate containing a lesion at a specific position. We found that DNA ligation is significantly slower than the preceding mitochondrial BER steps. Overexpression of DNA ligase III in mitochondria improved the rate of overall BER, increased cell survival after menadione induced oxidative stress and reduced autophagy following the inhibition of the mitochondrial electron transport chain complex I by rotenone. Our results suggest that the amount of DNA ligase III in mitochondria may be critical for cell survival following prolonged oxidative stress, and demonstrate a functional link between mitochondrial DNA damage and repair, cell survival upon oxidative stress, and removal of dysfunctional mitochondria by autophagy.
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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.