ReviewThe FEBS journal2017
Human mitochondrial nucleases.
Review in The FEBS journal, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 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
18 citing papers in PubMed, 30 citations in OpenAlex.
- Herpes simplex virus 1 subverts the mitochondrial network to support the infection: A lesson on mitochondrial versatility.bioRxiv : the preprint server for biology · 2026Article
- Mitochondrial DNA signals driving immune responses: Why, How, Where?Cell communication and signaling : CCS · 2025Review
- Mitochondria facilitate neuronal differentiation by metabolising nuclear-encoded RNA.Cell communication and signaling : CCS · 2024Article
- Light-strand bias and enriched zones of embedded ribonucleotides are associated with DNA replication and transcription in the human-mitochondrial genome.Nucleic acids research · 2024Article
- Human mtDNA-Encoded Long ncRNAs: Knotty Molecules and Complex Functions.International journal of molecular sciences · 2024Review
- Single-Nucleotide Polymorphisms in Genes Maintaining the Stability of Mitochondrial DNA Affect the Occurrence, Onset, Severity and Treatment of Major Depressive Disorder.International journal of molecular sciences · 2023Article
- Mitochondrial DNA Release in Innate Immune Signaling.Annual review of biochemistry · 2023Review
- Review
- Semi-in vitro detection of MgScientific reports · 2022Article
- Mitochondrial tRNA-Derived Fragments and Their Contribution to Gene Expression Regulation.Frontiers in physiology · 2021Review
- Functional Interplay between Cristae Biogenesis, Mitochondrial Dynamics and Mitochondrial DNA Integrity.International journal of molecular sciences · 2019Review
- A unique exonuclease ExoG cleaves between RNA and DNA in mitochondrial DNA replication.Nucleic acids research · 2019Article
- Modulation of mtDNA copy number ameliorates the pathological consequences of a heteroplasmic mtDNA mutation in the mouse.Science advances · 2019Article
- Mitochondrial DNA degradation: A quality control measure for mitochondrial genome maintenance and stress response.The Enzymes · 2019Review
- Linear mitochondrial DNA is rapidly degraded by components of the replication machinery.Nature communications · 2018Article
- Sensing the Stress: A Role for the UPRFrontiers in cell and developmental biology · 2018Review
- The MRPP1/MRPP2 complex is a tRNA-maturation platform in human mitochondria.Nucleic acids research · 2017Article
- Article
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 1 country.
Funding
Abstract
Mitochondria are cytosolic organelles that have many essential roles including ATP production via oxidative phosphorylation, apoptosis, iron-sulfur cluster biogenesis, heme and steroid synthesis, calcium homeostasis, and regulation of cellular redox state. One of the unique features of these organelles is the presence of an extrachromosomal mitochondrial genome (mtDNA), together with all the machinery required to replicate and transcribe mtDNA. The accurate maintenance of mitochondrial gene expression is essential for correct organellar metabolism, and is in part dependent on the levels of mtDNA and mtRNA, which are regulated by balancing synthesis against degradation. It is clear that although a number of mitochondrial nucleases have been identified, not all those responsible for the degradation of DNA or RNA have been characterized. Recent investigations, however, have revealed the contribution that mutations in the genes coding for these enzymes has made to causing pathogenic mitochondrial diseases.
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.