ArticleCell reports2021
NDUFS3 depletion permits complex I maturation and reveals TMEM126A/OPA7 as an assembly factor binding the ND4-module intermediate.
Article in Cell reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 33 citations in OpenAlex.
- Recessive variants in mitochondrial complex I nuclear subunits are an underrated cause of optic atrophy.Brain : a journal of neurology · 2026Article
- Complex I protein NDUFB9 is a metabolic vulnerability in triple negative breast cancer brain metastases.Nature communications · 2026Article
- Neurological manifestations and genotype-phenotype correlations inBrain communications · 2026Article
- Induced mitochondrial deficit by NDUFS3 transient silencing reduces RAB7 expression and causes lysosomal dysfunction in pancreatic cancer cells.Cell communication and signaling : CCS · 2025Article
- Pathogenic mitochondrial DNA variants are associated with response to anti-VEGF therapy in ovarian cancer PDX models.Journal of experimental & clinical cancer research : CR · 2024Article
- Molecular mechanisms of MAZ targeting up-regulation of NDUFS3 expression to promote malignant progression in melanoma.Communications biology · 2024Article
- Article
- Mitochondria in Retinal Ganglion Cells: Unraveling the Metabolic Nexus and Oxidative Stress.International journal of molecular sciences · 2024Review
- SRSF1 Is Required for Mitochondrial Homeostasis and Thermogenic Function in Brown Adipocytes Through its Control of Ndufs3 Splicing.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Using cryo-EM to understand the assembly pathway of respiratory complex I.Acta crystallographica. Section D, Structural biology · 2024Article
- Identification of TMEM126A as OXA1L-interacting protein reveals cotranslational quality control in mitochondria.Molecular cell · 2024Article
- The Italian reappraisal of the most frequent genetic defects in hereditary optic neuropathies and the global top 10.Brain : a journal of neurology · 2023Article
- Article
- Elucidation of the Role of FAM210B in Mitochondrial Metabolism and Erythropoiesis.Molecular and cellular biology · 2022Article
- NDUFS3 knockout cancer cells and molecular docking reveal specificity and mode of action of anti-cancer respiratory complex I inhibitors.Open biology · 2022Article
- MicroRNA and Metabolic Profiling of a Primary Ovarian Neuroendocrine Carcinoma Pulmonary-Type Reveals a High Degree of Similarity with Small Cell Lung Cancer.Non-coding RNA · 2022Article
- Inducing respiratory complex I impairment elicits an increase in PGC1α in ovarian cancer.Scientific reports · 2022Article
- Genetic spectrum and characteristics of autosomal optic neuropathy in Korean: Use of next-generation sequencing in suspected hereditary optic atrophy.Frontiers in neurology · 2022Article
- Mitochondrial Retinopathies.International journal of molecular sciences · 2021Review
- Molecular Mechanisms behind Inherited Neurodegeneration of the Optic Nerve.Biomolecules · 2021Review
Corrections and comments
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Authors and funding
12 authors at 4 institutions in 2 countries.
Funding
Abstract
Complex I (CI) is the largest enzyme of the mitochondrial respiratory chain, and its defects are the main cause of mitochondrial disease. To understand the mechanisms regulating the extremely intricate biogenesis of this fundamental bioenergetic machine, we analyze the structural and functional consequences of the ablation of NDUFS3, a non-catalytic core subunit. We show that, in diverse mammalian cell types, a small amount of functional CI can still be detected in the complete absence of NDUFS3. In addition, we determine the dynamics of CI disassembly when the amount of NDUFS3 is gradually decreased. The process of degradation of the complex occurs in a hierarchical and modular fashion in which the ND4 module remains stable and bound to TMEM126A. We, thus, uncover the function of TMEM126A, the product of a disease gene causing recessive optic atrophy as a factor necessary for the correct assembly and function of CI.
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