ArticleThe Journal of biological chemistry2013
Negative regulation of 26S proteasome stability via calpain-mediated cleavage of Rpn10 subunit upon mitochondrial dysfunction in neurons.
Article in The Journal of biological chemistry, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers, 1 of them a synthesis that pooled it.
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Who cites it
37 citing papers in PubMed, 1 synthesis or guideline pooled it, 59 citations in OpenAlex.
- Global research landscape and hotspots of paraptosis: a multi-database bibliometric analysis with a focused literature review.Frontiers in oncology · 2026Pooled it
- Respirometry-Based Screening of Marine Natural Products Identifies Leptochelin A as a Novel Modulator of Mitochondrial Function.Oxidative medicine and cellular longevity · 2026Article
- Activation of the 20S proteasome core particle prevents cell death induced by oxygen- and glucose deprivation in cultured cortical neurons.Apoptosis : an international journal on programmed cell death · 2025Article
- DNA-controlled protein fluorescence: Design of aptamer-split peptide hetero-modulator for GFP to respond to intracellular ATP levels.Nucleic acids research · 2024Article
- Mitochondrial Dysfunction and Protein Homeostasis in Aging: Insights from a Premature-Aging Mouse Model.Biomolecules · 2024Article
- Mechanisms of ubiquitin-independent proteasomal degradation and their roles in age-related neurodegenerative disease.Frontiers in cell and developmental biology · 2024Review
- Adult-Onset Deficiency of Mitochondrial Complex III in a Mouse Model of Alzheimer's Disease Decreases Amyloid Beta Plaque Formation.Molecular neurobiology · 2022Article
- Highly conserved shifts in ubiquitin-proteasome system (UPS) activity drive mitochondrial remodeling during quiescence.Nature communications · 2022Article
- Activation of the ubiquitin-proteasome system contributes to oculopharyngeal muscular dystrophy through muscle atrophy.PLoS genetics · 2022Article
- Protein Carbonylation: Emerging Roles in Plant Redox Biology and Future Prospects.Plants (Basel, Switzerland) · 2021Review
- Efficiency of the four proteasome subtypes to degrade ubiquitinated or oxidized proteins.Scientific reports · 2020Article
- The Nrf2/PGC1Oxidative medicine and cellular longevity · 2020Article
- Mitochondrial and calcium perturbations in rat CNS neurons induce calpain-cleavage of Parkin: Phosphatase inhibition stabilizes pSerBiochimica et biophysica acta. Molecular basis of disease · 2019Article
- Renal cold storage followed by transplantation impairs proteasome function and mitochondrial protein homeostasis.American journal of physiology. Renal physiology · 2019Article
- Small Molecule Modulation of Proteasome Assembly.Biochemistry · 2018Article
- Protein Modifications with Ubiquitin as Response to Cerebral Ischemia-Reperfusion Injury.Translational stroke research · 2018Review
- NGF-Dependent Changes in Ubiquitin Homeostasis Trigger Early Cholinergic Degeneration in Cellular and Animal AD-Model.Frontiers in cellular neuroscience · 2018Article
- Potential Alzheimer's Disease Therapeutics Among Weak Cysteine Protease Inhibitors Exhibit Mechanistic Differences Regarding Extent of Cathepsin B Up-Regulation and Ability to Block Calpain.European scientific journal · 2017Article
- The role of the immunoproteasome in interferon-γ-mediated microglial activation.Scientific reports · 2017Article
- Neurotoxic mechanisms by which the USP14 inhibitor IU1 depletes ubiquitinated proteins and Tau in rat cerebral cortical neurons: Relevance to Alzheimer's disease.Biochimica et biophysica acta. Molecular basis of disease · 2017Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Proteasomal and mitochondrial dysfunctions are implicated in chronic neurodegenerative diseases. To investigate the impact of mitochondrial impairment on the proteasome, we treated rat cerebral cortical neurons with oligomycin, antimycin, or rotenone, which inhibit different elements of the electron transport chain. Firstly, we observed a reduction in ubiquitinated proteins and E1 activity. Secondly, we established that 26S proteasomes are disassembled with a decline in activity. Thirdly, we show, to our knowledge for the first time, that calpain activation triggers the selective processing of the 26S proteasome subunit Rpn10. Other proteasome subunits tested were not affected. Calpain also cleaved caspase 3 to an inactive fragment, thus preventing apoptosis that is an energy-dependent cell death pathway. In addition, calpain cleaved the microtubule-associated protein Tau, a major component of neurofibrillary tangles in Alzheimer disease and other tauopathies. Fourthly, we detected a rise in 20S proteasome levels and activity. Finally, we show that both acute (16 h) and long term (up to 7 days) mitochondrial impairment led to down-regulation of ubiquitinated-proteins, 26S proteasome disassembly, and a rise in 20S proteasomes. We postulate that upon mitochondrial dysfunction, ATP depletion and calpain activation contribute to the demise of protein turnover by the ubiquitin/proteasome pathway. The concomitant rise in 20S proteasomes, which seem to degrade proteins in an unregulated and energy-independent manner, in the short term may carry out the turnover of randomly unfolded oxidized proteins. However, if chronic, it could lead to neurodegeneration as regulated protein degradation by the ubiquitin/proteasome pathway is essential for neuronal survival.
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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.