ArticleThe Journal of biological chemistry2010
Caspase-3 cleaves specific 19 S proteasome subunits in skeletal muscle stimulating proteasome activity.
Article in The Journal of biological chemistry, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
53 citing papers in PubMed, 87 citations in OpenAlex.
- Multilayer modulation of the proteasome: new strategies for neuroprotection.Frontiers in molecular neuroscience · 2026Article
- Beyond muscle weakness: pathogenesis of sepsis-induced myopathy and its management.Open medicine (Warsaw, Poland) · 2026Review
- Protein-energy wasting in chronic kidney disease: mechanisms responsible for loss of muscle mass and function.Kidney research and clinical practice · 2025Article
- Perspectives on the interpretation of mitochondrial responses during skeletal muscle disuse-induced atrophy.The Journal of physiology · 2025Review
- Mitochondrial Maintenance in Skeletal Muscle.Cold Spring Harbor perspectives in biology · 2025Review
- Impact of physical activity on physical function, mitochondrial energetics, ROS production, and CaCell reports. Medicine · 2025Article
- Lifelong dietary protein restriction induces denervation and skeletal muscle atrophy in mice.Free radical biology & medicine · 2024Article
- Musculoskeletal complications of Cushing syndrome.Reumatologia · 2023Review
- Maternal rodent exposure to di-(2-ethylhexyl) phthalate decreases muscle mass in the offspring by increasing myostatin.Journal of cachexia, sarcopenia and muscle · 2022Article
- Muscle Wasting in Chronic Kidney Disease: Mechanism and Clinical Implications-A Narrative Review.International journal of molecular sciences · 2022Review
- Pathophysiological mechanisms leading to muscle loss in chronic kidney disease.Nature reviews. Nephrology · 2022Review
- Integrating Mechanisms of Exacerbated Atrophy and Other Adverse Skeletal Muscle Impact in COPD.Frontiers in physiology · 2022Review
- Article
- Mitochondrial Dynamics and Mitophagy in Skeletal Muscle Health and Aging.International journal of molecular sciences · 2021Review
- Zinc at the crossroads of exercise and proteostasis.Redox biology · 2020Review
- Signaling Pathways That Control Muscle Mass.International journal of molecular sciences · 2020Review
- Exogenous miR-26a suppresses muscle wasting and renal fibrosis in obstructive kidney disease.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2019Article
- Uremic metabolites impair skeletal muscle mitochondrial energetics through disruption of the electron transport system and matrix dehydrogenase activity.American journal of physiology. Cell physiology · 2019Article
- Heterogeneous responses to low level death receptor activation are explained by random molecular assembly of the Caspase-8 activation platform.PLoS computational biology · 2019Article
- The ubiquitin-proteasome system in kidney physiology and disease.Nature reviews. Nephrology · 2019Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
With muscle wasting, caspase-3 activation and the ubiquitin-proteasome system act synergistically to increase the degradation of muscle proteins. Whether proteasome activity is also elevated in response to catabolic conditions is unknown. We find that caspase-3 increases proteasome activity in myotubes but not in myoblasts. This difference is related to the cleavage of specific 19 S proteasome subunits. In mouse muscle or myotubes, caspase-3 cleaves Rpt2 and Rpt6 increasing proteasome activity. In myoblasts, caspase-3 cleaves Rpt5 to decrease proteasome activity. To confirm the caspase-3 dependence, caspase-3 cleavage sites in Rpt2, Rpt6, or Rpt5 were mutated. This prevented the cleavage of these subunits by caspase-3 as well as the changes in proteasome activity. During differentiation of myoblasts to myotubes, there is an obligatory, transient increase in caspase-3 activity, accompanied by a corresponding increase in proteasome activity and cleavage of Rpt2 and Rpt6. Therefore, differentiation changes the proteasome type from sensitivity of Rpt5 to caspase-3 in myoblasts to sensitivity of Rpt2 and Rpt6 in myotubes. This novel mechanism identifies a feed-forward amplification that augments muscle proteolysis in catabolic conditions. Indeed, we found that in mice with a muscle wasting condition, chronic kidney disease, there was cleavage of subunits Rpt2 and Rpt6 and stimulation of proteasome activity.
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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.