ArticleNature communications2023
The assembly of the Mitochondrial Complex I Assembly complex uncovers a redox pathway coordination.
Article in Nature communications, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
What it found
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Who cites it
19 citing papers in PubMed, 24 citations in OpenAlex.
- Article
- Targeting the Mitochondrial Phenotype in Cockayne Syndrome Patient Cells: From Bioenergetic Fragility to Pharmacologic Rescue.bioRxiv : the preprint server for biology · 2026Article
- Moonlighting cytosolic function of ACAD9: suppression of TRAF6-mediated osteoclastogenesis and protection against osteoporosis.Cell death & disease · 2026Article
- Mitochondrial unfolded protein response as a central stress-integration hub: mechanisms and implications in disease contexts.Burns & trauma · 2026Review
- Mitochondrial dysfunction in hepatocellular carcinoma: from metabolism to targeted therapies.Molecular and cellular biochemistry · 2025Review
- PPARα-Mediated Fatty Acid Catabolism in Astrocytes Was Involved in Improvement of Cognitive Dysfunction by Phlorizin in APP/PS1 Mice.Antioxidants (Basel, Switzerland) · 2025Article
- TRAF6 integrates innate immune signals to regulate glucose homeostasis via Parkin-dependent and Parkin-independent mitophagy.Science advances · 2025Article
- Identification and Validation of Iron Metabolism-Related Biomarkers in Endometriosis: A Mendelian Randomization and Single-Cell Transcriptomics Study.Current issues in molecular biology · 2025Article
- Integrated Multi-Omics Analysis and Cross-Model Validation Reveal Mitochondrial Signatures in Alzheimer's Disease.CNS neuroscience & therapeutics · 2025Article
- A Late-Onset and Mild Phenotype of Mitochondrial Complex I Deficiency Due to a Novel Reported Variant Within theInternational journal of molecular sciences · 2025Article
- Mitochondrial dysfunction in the regulation of aging and aging-related diseases.Cell communication and signaling : CCS · 2025Review
- Hidden β-γ Dehydrogenation Products in Long-Chain Fatty Acid Oxidation Unveiled by NMR: Implications on Lipid Metabolism.ACS bio & med chem Au · 2025Article
- Structural bioinformatic study of human mitochondrial respiratory integral membrane megacomplex and its AlphaFold3 predicted water-soluble QTY megacomplex analog.QRB discovery · 2025Article
- Fine-Tuned Expression of Evolutionarily Conserved Signaling Molecules in theInternational journal of molecular sciences · 2024Article
- HADHA Regulates Respiratory Complex Assembly and Couples FAO and OXPHOS.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Review
- HINT2 protects against pressure overload-induced cardiac remodelling through mitochondrial pathways.Journal of cellular and molecular medicine · 2024Article
- Using cryo-EM to understand the assembly pathway of respiratory complex I.Acta crystallographica. Section D, Structural biology · 2024Article
- Neurotoxic β-amyloid oligomers cause mitochondrial dysfunction-the trigger for PANoptosis in neurons.Frontiers in aging neuroscience · 2024Review
Corrections and comments
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Authors and funding
13 authors at 4 institutions in 3 countries.
Funding
Abstract
The Mitochondrial Complex I Assembly (MCIA) complex is essential for the biogenesis of respiratory Complex I (CI), the first enzyme in the respiratory chain, which has been linked to Alzheimer's disease (AD) pathogenesis. However, how MCIA facilitates CI assembly, and how it is linked with AD pathogenesis, is poorly understood. Here we report the structural basis of the complex formation between the MCIA subunits ECSIT and ACAD9. ECSIT binding induces a major conformational change in the FAD-binding loop of ACAD9, releasing the FAD cofactor and converting ACAD9 from a fatty acid β-oxidation (FAO) enzyme to a CI assembly factor. We provide evidence that ECSIT phosphorylation downregulates its association with ACAD9 and is reduced in neuronal cells upon exposure to amyloid-β (Aβ) oligomers. These findings advance our understanding of the MCIA complex assembly and suggest a possible role for ECSIT in the reprogramming of bioenergetic pathways linked to Aβ toxicity, a hallmark of AD.
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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.