ArticleThe EMBO journal2022
AIFM1 is a component of the mitochondrial disulfide relay that drives complex I assembly through efficient import of NDUFS5.
Article in The EMBO journal, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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Who cites it
31 citing papers in PubMed, 45 citations in OpenAlex.
- Engineered flavonoid disrupts mitochondrial AIF/CHCHD4 complex for targeted cancer therapy.Acta pharmaceutica Sinica. B · 2026Article
- ALR couples IMS redox and heme biosynthesis beyond the disulfide relay.Science advances · 2026Article
- Disulfidptosis-Associated Neurotoxicity Induced by Cadmium Under an Environmentally Relevant Cadmium Exposure Scenario.International journal of molecular sciences · 2026Article
- Off-target anti-leukemic effects of antibiotics: mechanisms and therapeutic insights.Cancer chemotherapy and pharmacology · 2026Review
- Redox signals and oxidative stress in the control of mitochondrial protein import.Protein science : a publication of the Protein Society · 2026Review
- Cardiomyopathy and mitochondrial encephalomyopathy in a female child associated with a heterozygous X-linked AIFM1 variant.Molecular and cellular pediatrics · 2026Article
- Clean cut to curtail respiration: OMA1 cleaves AIFM1 to tune stress-induced bioenergetics.The EMBO journal · 2026Article
- Linking neurogenesis, oligodendrogenesis, and myelination defects to neurodevelopmental disruption in primary mitochondrial disorders.FEBS letters · 2026Review
- Stress-induced OMA1-mediated cleavage of AIFM1 suppresses cell growth by controlling mitochondrial OXPHOS activity.The EMBO journal · 2026Article
- Methylene blue restores NADJournal of orthopaedic translation · 2026Article
- Clinical and molecular characterization of a novel pathogenic AIFM1 E336K mutation connecting mitochondrial dysfunction and neurodegeneration.Cell communication and signaling : CCS · 2026Article
- Integrative PANoptosis-focused omics analysis uncovers GSDMC as a candidate biomarker in breast cancer.Frontiers in cell and developmental biology · 2026Article
- CRABS-ROC, A respirometry protocol for overcoming substrate limitations, reveals excess brain mitochondrial Complex I capacity.Free radical biology & medicine · 2025Article
- Dietary lipid content modifies wah-1/AIFM1-associated phenotypes via LRK-1 and DRP-1 expression in C. elegans.Nature communications · 2025Article
- Liquid-Liquid Phase Separation in Hereditary Hearing Loss.Neuroscience bulletin · 2025Review
- Interaction with AK2A links AIFM1 to cellular energy metabolism.Molecular cell · 2025Article
- Apoptosis-inducing factor (AIF) at the crossroad of cell survival and cell death: implications for cancer and mitochondrial diseases.Cell communication and signaling : CCS · 2025Review
- CHCHD4 Oxidoreductase Activity: A Comprehensive Analysis of the Molecular, Functional, and Structural Properties of Its Redox-Regulated Substrates.Molecules (Basel, Switzerland) · 2025Review
- Chemical Proteomics Reveals Human Off-Targets of Fluoroquinolone Induced Mitochondrial Toxicity.Angewandte Chemie (International ed. in English) · 2025Article
- Redox regulation: mechanisms, biology and therapeutic targets in diseases.Signal transduction and targeted therapy · 2025Review
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Authors and funding
24 authors at 4 institutions in 4 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The mitochondrial intermembrane space protein AIFM1 has been reported to mediate the import of MIA40/CHCHD4, which forms the import receptor in the mitochondrial disulfide relay. Here, we demonstrate that AIFM1 and MIA40/CHCHD4 cooperate beyond this MIA40/CHCHD4 import. We show that AIFM1 and MIA40/CHCHD4 form a stable long-lived complex in vitro, in different cell lines, and in tissues. In HEK293 cells lacking AIFM1, levels of MIA40 are unchanged, but the protein is present in the monomeric form. Monomeric MIA40 neither efficiently interacts with nor mediates the import of specific substrates. The import defect is especially severe for NDUFS5, a subunit of complex I of the respiratory chain. As a consequence, NDUFS5 accumulates in the cytosol and undergoes rapid proteasomal degradation. Lack of mitochondrial NDUFS5 in turn results in stalling of complex I assembly. Collectively, we demonstrate that AIFM1 serves two overlapping functions: importing MIA40/CHCHD4 and constituting an integral part of the disulfide relay that ensures efficient interaction of MIA40/CHCHD4 with specific substrates.
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