ArticleThe Journal of biological chemistry2008
Identification of the mitochondrial ND3 subunit as a structural component involved in the active/deactive enzyme transition of respiratory complex I.
Article in The Journal of biological chemistry, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 76 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
76 citing papers in PubMed.
- Clinical Spectrum, Heteroplasmy-Phenotype Correlation, and Prognosis of the MT-ND3 m.10191 T > C Mutation.CNS neuroscience & therapeutics · 2026Article
- Mitochondrial complex III-derived ROS amplify immunometabolic changes in astrocytes and promote dementia pathology.Nature metabolism · 2025Article
- Global conformations ofScience advances · 2025Article
- Low oxidative stress during mitochondrial recovery from anoxia in Artemia franciscana, an invertebrate extremophile.Journal of comparative physiology. B, Biochemical, systemic, and environmental physiology · 2025Article
- MSCs-EVs harboring OA immune memory reprogram macrophage phenotype via modulation of the mt-ND3/NADH-CoQ axis for OA treatment.Journal of nanobiotechnology · 2025Article
- Proton-Translocating NADH-Ubiquinone Oxidoreductase: Interaction with Artificial Electron Acceptors, Inhibitors, and Potential Medicines.International journal of molecular sciences · 2024Review
- Using cryo-EM to understand the assembly pathway of respiratory complex I.Acta crystallographica. Section D, Structural biology · 2024Article
- Resting mitochondrial complex I fromeLife · 2023Article
- Article
- Making the leap from structure to mechanism: are the open states of mammalian complex I identified by cryoEM resting states or catalytic intermediates?Current opinion in structural biology · 2022Review
- Conformational changes in mitochondrial complex I of the thermophilic eukaryoteScience advances · 2022Article
- Insights into complex I assembly: Function of NDUFAF1 and a link with cardiolipin remodeling.Science advances · 2022Article
- Next-generation sequencing of Tunisian Leigh syndrome patients reveals novel variations: impact for diagnosis and treatment.Bioscience reports · 2022Article
- ND3 Cys39 in complex I is exposed during mitochondrial respiration.Cell chemical biology · 2022Article
- Reverse Electron Transfer by Respiratory Complex I Catalyzed in a Modular Proteoliposome System.Journal of the American Chemical Society · 2022Article
- The coupling mechanism of mammalian mitochondrial complex I.Nature structural & molecular biology · 2022Article
- Novel Mutation m.10372A>G inNeurology. Genetics · 2021Article
- Generation of Reactive Oxygen Species by Mitochondria.Antioxidants (Basel, Switzerland) · 2021Review
- Proteomic analysis reveals ginsenoside Rb1 attenuates myocardial ischemia/reperfusion injury through inhibiting ROS production from mitochondrial complex I.Theranostics · 2021Article
- Essential role of accessory subunit LYRM6 in the mechanism of mitochondrial complex I.Nature communications · 2020Article
16 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors.
Funding
Abstract
Mitochondrial complex I (NADH:ubiquinone oxidoreductase) undergoes reversible deactivation upon incubation at 30-37 degrees C. The active/deactive transition could play an important role in the regulation of complex I activity. It has been suggested recently that complex I may become modified by S-nitrosation under pathological conditions during hypoxia or when the nitric oxide:oxygen ratio increases. Apparently, a specific cysteine becomes accessible to chemical modification only in the deactive form of the enzyme. By selective fluorescence labeling and proteomic analysis, we have identified this residue as cysteine-39 of the mitochondrially encoded ND3 subunit of bovine heart mitochondria. Cysteine-39 is located in a loop connecting the first and second transmembrane helix of this highly hydrophobic subunit. We propose that this loop connects the ND3 subunit of the membrane arm with the PSST subunit of the peripheral arm of complex I, placing it in a region that is known to be critical for the catalytic mechanism of complex I. In fact, mutations in three positions of the loop were previously reported to cause Leigh syndrome with and without dystonia or progressive mitochondrial disease.
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.