ArticleJournal of translational genetics and genomics2020
Mitochondrial translation defects and human disease.
Article in Journal of translational genetics and genomics, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 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.
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.
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Who cites it
11 citing papers in PubMed, 25 citations in OpenAlex.
- Structural basis of TACO1-mediated efficient mitochondrial translation.Nature communications · 2026Article
- Structural Basis of TACO1-Mediated Efficient Mitochondrial Translation.bioRxiv : the preprint server for biology · 2025Article
- Emerging mechanisms of human mitochondrial translation regulation.Trends in biochemical sciences · 2025Review
- The sequence variation of mitochondrial tRNA tyrosine and cysteine among Iranian women with idiopathic recurrent miscarriage: A case-control study.International journal of reproductive biomedicine · 2023Article
- Cytosolic and mitochondrial translation elongation are coordinated through the molecular chaperone TRAP1 for the synthesis and import of mitochondrial proteins.Genome research · 2023Article
- Leigh syndrome is the main clinical characteristic of PTCD3 deficiency.Brain pathology (Zurich, Switzerland) · 2023Article
- Bilateral deafness, diabetes, and different types of cardiomyopathy in family members with m.3243A > g mutation: a case report.European heart journal. Case reports · 2023Article
- A Genome-Wide Functional Screen Identifies Enhancer and Protective Genes for Amyloid Beta-Peptide Toxicity.International journal of molecular sciences · 2023Article
- Clinical and bi-genomic DNA findings of patients suspected to have mitochondrial diseases.Frontiers in genetics · 2023Article
- Mito-FUNCAT-FACS reveals cellular heterogeneity in mitochondrial translation.RNA (New York, N.Y.) · 2022Article
- Mitochondrial tRNA-Derived Fragments and Their Contribution to Gene Expression Regulation.Frontiers in physiology · 2021Review
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 1 institution in 1 country.
Funding
Abstract
In eukaryotic cells, mitochondria perform the essential function of producing cellular energy in the form of ATP via the oxidative phosphorylation system. This system is composed of 5 multimeric protein complexes of which 13 protein subunits are encoded by the mitochondrial genome: Complex I (7 subunits), Complex III (1 subunit),Complex IV (3 subunits), and Complex (2 subunits). Effective mitochondrial translation is necessary to produce the protein subunits encoded by the mitochondrial genome (mtDNA). Defects in mitochondrial translation are known to cause a wide variety of clinical disease in humans with high-energy consuming organs generally most prominently affected. Here, we review several classes of disease resulting from defective mitochondrial translation including disorders with mitochondrial tRNA mutations, mitochondrial aminoacyl-tRNA synthetase disorders, mitochondrial rRNA mutations, and mitochondrial ribosomal protein disorders.
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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.