ReviewJournal of inherited metabolic disease2015
Mitochondrial transcript maturation and its disorders.
Review in Journal of inherited metabolic disease, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 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
51 citing papers in PubMed, 77 citations in OpenAlex.
- Role of mitochondrial translation in modulating inflammatory disease outcome: Current knowledge and future perspectives.The Journal of biological chemistry · 2026Review
- Nuclear genetic modulation of tissue-specific mitochondrial RNA processing contributes to common disease risk.Nature communications · 2026Article
- Pathogenic human mitochondrial tRNA variants impair RNA processing by compromising 5' leader removal.bioRxiv : the preprint server for biology · 2026Article
- The molecular machinery for maturation of primary mtDNA transcripts.Human molecular genetics · 2024Review
- A novel mutation inHeliyon · 2024Article
- Genetic Networks of Alzheimer's Disease, Aging, and Longevity in Humans.International journal of molecular sciences · 2023Article
- ANGEL2 phosphatase activity is required for non-canonical mitochondrial RNA processing.Nature communications · 2022Article
- Mutational Analysis and mtDNA Haplogroup Characterization in Three Serbian Cases of Mitochondrial Encephalomyopathies and Literature Review.Diagnostics (Basel, Switzerland) · 2021Article
- Human Mitochondrial RNA Processing and Modifications: Overview.International journal of molecular sciences · 2021Review
- Engineering Genetic Systems for Treating Mitochondrial Diseases.Pharmaceutics · 2021Review
- Ablation of Mto1 in zebrafish exhibited hypertrophic cardiomyopathy manifested by mitochondrion RNA maturation deficiency.Nucleic acids research · 2021Article
- Monitoring mitochondrial translation in living cells.EMBO reports · 2021Article
- Human GTPBP5 is involved in the late stage of mitoribosome large subunit assembly.Nucleic acids research · 2021Article
- Reconstitution of mammalian mitochondrial translation system capable of correct initiation and long polypeptide synthesis from leaderless mRNA.Nucleic acids research · 2021Article
- Mitochondrial Nucleic Acid as a Driver of Pathogenic Type I Interferon Induction in Mendelian Disease.Frontiers in immunology · 2021Review
- Novel Mutations in theFrontiers in genetics · 2021Article
- Epigenetics of Animal Personality: DNA Methylation Cannot Explain the Heritability of Exploratory Behavior in a Songbird.Integrative and comparative biology · 2020Article
- Asymmetrical effects of deafness-associated mitochondrial DNA 7516delA mutation on the processing of RNAs in the H-strand and L-strand polycistronic transcripts.Nucleic acids research · 2020Article
- Phase-separated bacterial ribonucleoprotein bodies organize mRNA decay.Wiley interdisciplinary reviews. RNA · 2020Review
- Ccm1p is a 15S rRNA primary transcript processing factor as elucidated by a novel in vivo system in Saccharomyces cerevisiae.Current genetics · 2020Article
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 2 countries.
Funding
Abstract
Mitochondrial respiratory chain deficiencies exhibit a wide spectrum of clinical presentations owing to defective mitochondrial energy production through oxidative phosphorylation. These defects can be caused by either mutations in the mitochondrial DNA (mtDNA) or mutations in nuclear genes coding for mitochondrially-targeted proteins. The underlying pathomechanisms can affect numerous pathways involved in mitochondrial biology including expression of mtDNA-encoded genes. Expression of the mitochondrial genes is extensively regulated at the post-transcriptional stage and entails nucleolytic cleavage of precursor RNAs, RNA nucleotide modifications, RNA polyadenylation, RNA quality and stability control. These processes ensure proper mitochondrial RNA (mtRNA) function, and are regulated by dedicated, nuclear-encoded enzymes. Recent growing evidence suggests that mutations in these nuclear genes, leading to incorrect maturation of RNAs, are a cause of human mitochondrial disease. Additionally, mutations in mtDNA-encoded genes may also affect RNA maturation and are frequently associated with human disease. We review the current knowledge on a subset of nuclear-encoded genes coding for proteins involved in mitochondrial RNA maturation, for which genetic variants impacting upon mitochondrial pathophysiology have been reported. Also, primary pathological mtDNA mutations with recognised effects upon RNA processing are described.
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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.