ArticleAmerican journal of physiology. Regulatory, integrative and comparative physiology2011
Mre11 is expressed in mammalian mitochondria where it binds to mitochondrial DNA.
Article in American journal of physiology. Regulatory, integrative and comparative physiology, 2011. 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, 44 citations in OpenAlex.
- Persistence of large mtDNA rearrangements linked to premature aging in Pol γ exonuclease-deficient mice.Nucleic acids research · 2026Article
- To cleave or not and how? The DNA exonucleases and endonucleases in immunity.Genes & diseases · 2025Review
- The multifaceted functions of DNA-PKcs: implications for the therapy of human diseases.MedComm · 2024Review
- DNA Double Strand Break and Response Fluorescent Assays: Choices and Interpretation.International journal of molecular sciences · 2024Review
- Article
- REC drives recombination to repair double-strand breaks in animal mtDNA.The Journal of cell biology · 2023Article
- Targeting Mre11 overcomes platinum resistance and induces synthetic lethality in XRCC1 deficient epithelial ovarian cancers.NPJ precision oncology · 2022Article
- MRE11-dependent instability in mitochondrial DNA fork protection activates a cGAS immune signaling pathway.Science advances · 2021Article
- Untangling the clinicopathological significance of MRE11-RAD50-NBS1 complex in sporadic breast cancers.NPJ breast cancer · 2021Article
- Natural and Artificial Mechanisms of Mitochondrial Genome Elimination.Life (Basel, Switzerland) · 2021Review
- Mechanisms of replication and repair in mitochondrial DNA deletion formation.Nucleic acids research · 2020Review
- Review
- Mitochondrial DNA: Epigenetics and environment.Environmental and molecular mutagenesis · 2019Review
- Mitochondrial DNA degradation: A quality control measure for mitochondrial genome maintenance and stress response.The Enzymes · 2019Review
- Homologous recombination-mediated repair of DNA double-strand breaks operates in mammalian mitochondria.Cellular and molecular life sciences : CMLS · 2018Article
- Linear mitochondrial DNA is rapidly degraded by components of the replication machinery.Nature communications · 2018Article
- DNA damage related crosstalk between the nucleus and mitochondria.Free radical biology & medicine · 2017Review
- Microhomology-mediated end joining is the principal mediator of double-strand break repair during mitochondrial DNA lesions.Molecular biology of the cell · 2016Article
- Protecting the mitochondrial powerhouse.Trends in cell biology · 2015Review
- Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 2 countries.
Funding
Abstract
Mre11 is a critical participant in upkeep of nuclear DNA, its repair, replication, meiosis, and maintenance of telomeres. The upkeep of mitochondrial DNA (mtDNA) is less well characterized, and whether Mre11 participates has been unknown. We previously found that high NaCl causes some of the Mre11 to leave the nucleus, but we did not then attempt to localize it within the cytoplasm. In the present studies, we find Mre11 in mitochondria isolated from primary renal cells and show that the amount of Mre11 in mitochondria increases with elevation of extracellular NaCl. We confirm the presence of Mre11 in the mitochondria of cells by confocal microscopy and show that some of the Mre11 colocalizes with mtDNA. Furthermore, crosslinking of Mre11 to DNA followed by Mre11 immunoprecipitation directly demonstrates that some Mre11 binds to mtDNA. Abundant Mre11 is also present in tissue sections from normal mouse kidneys, colocalized with mitochondria of proximal tubule and thick ascending limb cells. To explore whether distribution of Mre11 changes with cell differentiation, we used an experimental model of tubule formation by culturing primary kidney cells in Matrigel matrix. In nondifferentiated cells, Mre11 is mostly in the nucleus, but it becomes mostly cytoplasmic upon cell differentiation. We conclude that Mre11 is present in mitochondria where it binds to mtDNA and that the amount in mitochondria varies depending on cellular stress and differentiation. Our results suggest a role for Mre11 in the maintenance of genome integrity in mitochondria in addition to its previously known role in maintenance of nuclear DNA.
Indexed as
Identifiers
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.