ReviewLife (Basel, Switzerland)2020
Analysis of Human Mutations in the Supernumerary Subunits of Complex I.
Review in Life (Basel, Switzerland), 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 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
13 citing papers in PubMed, 16 citations in OpenAlex.
- Prolonged linezolid therapy induces progressive mitochondrial dysfunction in human peripheral blood mononuclear cells.Journal of translational medicine · 2026Article
- Identification of Intronic Variants inNeurology. Genetics · 2026Article
- Current perspectives on circadian regulation of mitochondrial dynamics in mood disorders and perioperative stress.Frontiers in pharmacology · 2026Review
- Global conformations ofScience advances · 2025Article
- NDUFA10-Mediated ATP Reduction in Medial Prefrontal Cortex Exacerbates Burst Suppression in Aged Mice.CNS neuroscience & therapeutics · 2025Article
- Mitochondrial Complex I Inhibition in Dopaminergic Neurons Causes Altered Protein Profile and Protein Oxidation: Implications for Parkinson's disease.Neurochemical research · 2023Article
- A Novel Mutation Associated with Neonatal Lethal Cardiomyopathy Leads to an Alternative Transcript Expression in the X-Linked Complex IInternational journal of molecular sciences · 2023Article
- Article
- Analysis of Human Clinical Mutations of Mitochondrial ND1 in a Bacterial Model System for Complex I.Life (Basel, Switzerland) · 2022Article
- Human clinical mutations in mitochondrially encoded subunits of Complex I can be successfully modeled in E. coli.Mitochondrion · 2022Article
- Impaired Mitochondrial Bioenergetics under Pathological Conditions.Life (Basel, Switzerland) · 2022Article
- Tackling Dysfunction of Mitochondrial Bioenergetics in the Brain.International journal of molecular sciences · 2021Review
- Accessory Subunits of the Matrix Arm of Mitochondrial Complex I with a Focus on Subunit NDUFS4 and Its Role in Complex I Function and Assembly.Life (Basel, Switzerland) · 2021Review
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Complex I is the largest member of the electron transport chain in human mitochondria. It comprises 45 subunits and requires at least 15 assembly factors. The subunits can be divided into 14 "core" subunits that carry out oxidation-reduction reactions and proton translocation, as well as 31 additional supernumerary (or accessory) subunits whose functions are less well known. Diminished levels of complex I activity are seen in many mitochondrial disease states. This review seeks to tabulate mutations in the supernumerary subunits of humans that appear to cause disease. Mutations in 20 of the supernumerary subunits have been identified. The mutations were analyzed in light of the tertiary and quaternary structure of human complex I (PDB id = 5xtd). Mutations were found that might disrupt the folding of that subunit or that would weaken binding to another subunit. In some cases, it appeared that no protein was made or, at least, could not be detected. A very common outcome is the lack of assembly of complex I when supernumerary subunits are mutated or missing. We suggest that poor assembly is the result of disrupting the large network of subunit interactions that the supernumerary subunits typically engage in.
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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.