ArticleThe Journal of biological chemistry2009
Mitochondrial DNA damage initiates a cell cycle arrest by a Chk2-associated mechanism in mammalian cells.
Article in The Journal of biological chemistry, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
What it found
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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
24 citing papers in PubMed, 57 citations in OpenAlex.
- Elevated levels of plasma mitochondrial DNA DAMPs are linked to clinical outcome in severely injured human subjects.Annals of surgery · 2013Trial
- FAM43A coordinates mtDNA replication and mitochondrial biogenesis in response to mtDNA depletion.The Journal of cell biology · 2025Article
- Exploring the oncogenic impact of heteroplasmicMitochondrial communications · 2025Article
- CHEK2 signaling is the key regulator of oocyte survival after chemotherapy.Science advances · 2023Article
- Mitochondrial PARP1 regulates NADExperimental & molecular medicine · 2022Article
- Small Heat Shock Proteins Collaborate with FAIM to Prevent Accumulation of Misfolded Protein Aggregates.International journal of molecular sciences · 2022Article
- A mitochondria-targeted caffeic acid derivative reverts cellular and mitochondrial defects in human skin fibroblasts from male sporadic Parkinson's disease patients.Redox biology · 2021Article
- Comprehensive molecular characterization of mitochondrial genomes in human cancers.Nature genetics · 2020Article
- Mitochondrial Impairment by Cyanine-Based Small Molecules Induces Apoptosis in Cancer Cells.ACS medicinal chemistry letters · 2020Article
- FAIM Is a Non-redundant Defender of Cellular Viability in the Face of Heat and Oxidative Stress and Interferes With Accumulation of Stress-Induced Protein Aggregates.Frontiers in molecular biosciences · 2020Article
- ROS and the DNA damage response in cancer.Redox biology · 2019Review
- Impairing Powerhouse in Colon Cancer Cells by Hydrazide-Hydrazone-Based Small Molecule.ACS omega · 2018Article
- Transcriptomic analysis of mitochondrial TFAM depletion changing cell morphology and proliferation.Scientific reports · 2017Article
- Mitochondrial DNA Damage Initiates Acute Lung Injury and Multi-Organ System Failure Evoked in Rats by Intra-Tracheal Pseudomonas Aeruginosa.Shock (Augusta, Ga.) · 2017Article
- Bcl-2 delays cell cycle through mitochondrial ATP and ROS.Cell cycle (Georgetown, Tex.) · 2017Article
- Evidence that bacteriophage λ lysogens may induce in response to the proton motive force uncoupler CCCP.FEMS microbiology letters · 2016Article
- Mitochondrially targeted Endonuclease III has a powerful anti-infarct effect in an in vivo rat model of myocardial ischemia/reperfusion.Basic research in cardiology · 2015Article
- CHK2 kinase in the DNA damage response and beyond.Journal of molecular cell biology · 2014Review
- Mitochondria in lung biology and pathology: more than just a powerhouse.American journal of physiology. Lung cellular and molecular physiology · 2014Review
- Mitochondria as a target of environmental toxicants.Toxicological sciences : an official journal of the Society of Toxicology · 2013Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Previous work from our laboratory has focused on mitochondrial DNA (mtDNA) repair and cellular viability. However, other events occur prior to the initiation of apoptosis in cells. Because of the importance of mtDNA in ATP production and of ATP in fuel cell cycle progression, we asked whether mtDNA damage was an upstream signal leading to cell cycle arrest. Using quantitative alkaline Southern blot technology, we found that exposure to menadione produced detectable mtDNA damage in HeLa cells that correlated with an S phase cell cycle arrest. To determine whether mtDNA damage was causatively linked to the observed cell cycle arrest, experiments were performed utilizing a MTS-hOGG1-Tat fusion protein to target the hOGG1 repair enzyme to mitochondria and enhance mtDNA repair. The results revealed that the transduction of MTS-hOGG1-Tat into HeLa cells alleviated the cell cycle block following an oxidative insult. Furthermore, mechanistic studies showed that Chk2 phosphorylation was enhanced following menadione exposure. Treatment of the HeLa cells with the hOGG1 fusion protein prior to menadione exposure resulted in an increase in the rate of Chk2 dephosphorylation. These results strongly support a direct link between mtDNA damage and cell cycle arrest.
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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.