ArticleThe Journal of biological chemistry2015
Cox17 Protein Is an Auxiliary Factor Involved in the Control of the Mitochondrial Contact Site and Cristae Organizing System.
Article in The Journal of biological chemistry, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 51 citations in OpenAlex.
- Copper, cuproptosis, and cancer: biology concepts of a novel cell death.Apoptosis : an international journal on programmed cell death · 2026Review
- Copper homeostasis and cuproptosis: molecular mechanisms and therapeutic opportunities.Molecular biomedicine · 2026Review
- MICOS and MIMAS, multifunctional assemblies linking mitochondrial biogenesis, architecture, and function.Protein science : a publication of the Protein Society · 2026Review
- Review
- Mutant CHCHD10 disrupts cytochrome c oxidation and activates mitochondrial retrograde signaling.EMBO molecular medicine · 2026Article
- Transcriptomics combined with metabolomics to elucidate the mechanisms of bacterial otitis media infection: insights from mitochondrial dysfunction.BMC microbiology · 2026Article
- Distinct signaling mechanisms and proteome phenotypes are elicited by compartment-specific genetic defects of copper homeostasis.bioRxiv : the preprint server for biology · 2026Article
- Copper homeostasis in macrophages: regulatory mechanisms and immunological implications.Frontiers in chemistry · 2026Review
- Association of Copper with Atherosclerosis and Treatment Strategies.Journal of cardiovascular translational research · 2025Review
- Mitochondrial cristae remodeling: Mechanisms, functions, and pathology.Cell insight · 2025Review
- The molecular mechanism and therapeutic landscape of copper and cuproptosis in cancer.Signal transduction and targeted therapy · 2025Review
- Copper in cancer: friend or foe? Metabolism, dysregulation, and therapeutic opportunities.Cancer communications (London, England) · 2025Review
- From copper homeostasis to cuproptosis: a new perspective on CNS immune regulation and neurodegenerative diseases.Frontiers in neurology · 2025Review
- The Role of Astrocytic Mitochondria in the Pathogenesis of Brain Ischemia.Molecular neurobiology · 2024Review
- Diabetic Cardiomyopathy and Cell Death: Focus on Metal-Mediated Cell Death.Cardiovascular toxicology · 2024Review
- Targeting cuproptosis with nano material: new way to enhancing the efficacy of immunotherapy in colorectal cancer.Frontiers in pharmacology · 2024Review
- COX17 acetylation via MOF-KANSL complex promotes mitochondrial integrity and function.Nature metabolism · 2023Article
- Copper-catalyzed dicarbonyl stress in NAFLD mice: protective effects of Oleuropein treatment on liver damage.Nutrition & metabolism · 2022Article
- Prime Real Estate: Metals, Cofactors and MICOS.Frontiers in cell and developmental biology · 2022Review
- Discovery of bactericides as an acute mitochondrial membrane damage inducer.Molecular biology of the cell · 2021Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The mitochondrial contact site and cristae organizing system (MICOS) is a recently discovered protein complex that is crucial for establishing and maintaining the proper inner membrane architecture and contacts with the outer membrane of mitochondria. The ways in which the MICOS complex is assembled and its integrity is regulated remain elusive. Here, we report a direct link between Cox17, a protein involved in the assembly of cytochrome c oxidase, and the MICOS complex. Cox17 interacts with Mic60, thereby modulating MICOS complex integrity. This interaction does not involve Sco1, a partner of Cox17 in transferring copper ions to cytochrome c oxidase. However, the Cox17-MICOS interaction is regulated by copper ions. We propose that Cox17 is a newly identified factor involved in maintaining the architecture of the MICOS complex.
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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.