ArticleBiomolecules2023
Insulin-Degrading Enzyme Interacts with Mitochondrial Ribosomes and Respiratory Chain Proteins.
Article in Biomolecules, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 6 citations in OpenAlex.
- Review
- Proteomic Analysis of Regulated Dendritic Cell Endosomes Reveals Dynamic Adaptation to Antigen Uptake and Cross-Presentation.European journal of immunology · 2026Article
- Insulin-Degrading Enzyme Regulates mRNA Processing and May Interact with the CCR4-NOT Complex.Cells · 2025Article
- Potential Mitochondria-Related Key Genes in Post-Traumatic Stress Disorder Analyzed by Machine Learning Methods.Neuropsychiatric disease and treatment · 2025Article
- Inhibition of insulin degrading enzyme suppresses osteoclast hyperactivity via enhancing Nrf2-dependent antioxidant response in glucocorticoid-induced osteonecrosis of the femoral head.Molecular medicine (Cambridge, Mass.) · 2024Article
- Loss of WDR23 proteostasis impacts mitochondrial homeostasis in the mouse brain.Cellular signalling · 2024Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Insulin-degrading enzyme (IDE) is a highly conserved metalloprotease that is mainly localized in the cytosol. Although IDE can degrade insulin and some other low molecular weight substrates efficiently, its ubiquitous expression suggests additional functions supported by experimental findings, such as a role in stress responses and cellular protein homeostasis. The translation of a long full-length IDE transcript has been reported to result in targeting to mitochondria, but the role of IDE in this compartment is unknown. To obtain initial leads on the function of IDE in mitochondria, we used a proximity biotinylation approach to identify proteins interacting with wild-type and protease-dead IDE targeted to the mitochondrial matrix. We find that IDE interacts with multiple mitochondrial ribosomal proteins as well as with proteins involved in the synthesis and assembly of mitochondrial complex I and IV. The mitochondrial interactomes of wild type and mutant IDE are highly similar and do not reveal any likely proteolytic IDE substrates. We speculate that IDE could adopt similar additional non-proteolytic functions in mitochondria as in the cytosol, acting as a chaperone and contributing to protein homeostasis and stress responses.
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Registered trials
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