ReviewAmerican journal of physiology. Cell physiology2023
A critical discussion on the relationship between E3 ubiquitin ligases, protein degradation, and skeletal muscle wasting: it's not that simple.
Review in American journal of physiology. Cell physiology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 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.
The trial behind it
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
26 citing papers in PubMed, 29 citations in OpenAlex.
- Multi-omics identifies promoter methylation and gene expression changes associated with human skeletal muscle atrophy.Experimental physiology · 2026Article
- Iron homeostasis disruption and lipid peroxidation in skeletal muscle during short-term immobilization.FEBS open bio · 2026Article
- Understanding cachexia and muscle dysfunction in the context of metastatic breast cancer.Cancer metastasis reviews · 2026Review
- Deubiquitinase YOD1 Inhibition Suppresses DEX- and Denervation-Induced Muscle Atrophy Through MAFbx Destabilization.Journal of cachexia, sarcopenia and muscle · 2026Article
- Pro-inflammatory cytokine-driven molecular signaling in skeletal muscle during cancer cachexia.Biochemical Society transactions · 2026Review
- ANKRD9 negatively regulates chicken myogenesis through ubiquitin-mediated regulation of IMPDH2.Poultry science · 2026Article
- Mechanisms of protein degradation in atrophying muscles: What have we learned during the past decade?The Journal of biological chemistry · 2026Review
- Exercise-specific post-translational modification signatures: unveiling precise regulatory mechanisms of molecular exercise language and cellular adaptation.Frontiers in sports and active living · 2026Review
- PTM encoding: decoding the mechanisms of exercise-induced metabolic memory through spatiotemporal modification networks.Frontiers in sports and active living · 2026Review
- Integrative Transcriptomics Identifies Ubiquitination-Related GenesJournal of inflammation research · 2026Article
- Response of UBR-box E3 ubiquitin ligases and protein quality control pathways to perturbations in protein synthesis and skeletal muscle size.American journal of physiology. Cell physiology · 2025Article
- Stigmasterol Protects Against Dexamethasone-Induced Muscle Atrophy by Modulating the FoxO3-MuRF1/MAFbx Signaling Pathway in C2C12 Myotubes and Mouse Skeletal Muscle.Biomolecules · 2025Article
- Response of UBR-box E3 ubiquitin ligases and protein quality control pathways to perturbations in protein synthesis and skeletal muscle size.bioRxiv : the preprint server for biology · 2025Article
- UBR5: A New Player in Protein Quality Control for Skeletal Muscle Growth and Remodeling.Exercise and sport sciences reviews · 2025Review
- Latest Updates on Sarcopenia and Cachexia: Insights from the 17th Sarcopenia, Cachexia, and Wasting Disorders Conference.Journal of bone metabolism · 2025Article
- The flux of energy in critical illness and the obesity paradox.Physiological reviews · 2025Review
- Muscle peripheral circadian clock drives nocturnal protein degradation via raised Ror/Rev-erb balance and prevents premature sarcopenia.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- A history of omics discoveries reveals the correlates and mechanisms of loading-induced hypertrophy in adult skeletal muscle. 2024 CaMPS young investigator award invited review.American journal of physiology. Cell physiology · 2025Review
- Muscle wasting in cancer cachexia: Mechanisms and the role of exercise.Experimental physiology · 2025Review
- Skeletal muscle atrophy induced by aging and disuse atrophy are strongly associated with the upregulation of the endoplasmic stress protein CHOP in rats.Molecular biology reports · 2025Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
Abstract
Ubiquitination is an important post-translational modification (PTM) for protein substrates, whereby ubiquitin is added to proteins through the coordinated activity of activating (E1), ubiquitin-conjugating (E2), and ubiquitin ligase (E3) enzymes. The E3s provide key functions in the recognition of specific protein substrates to be ubiquitinated and aid in determining their proteolytic or nonproteolytic fates, which has led to their study as indicators of altered cellular processes. MuRF1 and MAFbx/Atrogin-1 were two of the first E3 ubiquitin ligases identified as being upregulated in a range of different skeletal muscle atrophy models. Since their discovery, the expression of these E3 ubiquitin ligases has often been studied as a surrogate measure of changes to bulk protein degradation rates. However, emerging evidence has highlighted the dynamic and complex regulation of the ubiquitin proteasome system (UPS) in skeletal muscle and demonstrated that protein ubiquitination is not necessarily equivalent to protein degradation. These observations highlight the potential challenges of quantifying E3 ubiquitin ligases as markers of protein degradation rates or ubiquitin proteasome system (UPS) activation. This perspective examines the usefulness of monitoring E3 ubiquitin ligases for determining specific or bulk protein degradation rates in the settings of skeletal muscle atrophy. Specific questions that remain unanswered within the skeletal muscle atrophy field are also identified, to encourage the pursuit of new research that will be critical in moving forward our understanding of the molecular mechanisms that govern protein function and degradation in muscle.
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What OpenQuestion holds
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.