ArticleProceedings of the National Academy of Sciences of the United States of America2008
Glucocorticoids differentially regulate degradation of MyoD and Id1 by N-terminal ubiquitination to promote muscle protein catabolism.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.
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Who cites it
38 citing papers in PubMed, 67 citations in OpenAlex.
- Lycopene Increases Skeletal Muscle Mass by Promoting Myoblast Differentiation.Food science & nutrition · 2026Article
- Glucocorticoids Modulate Expression of Perineuronal Net Component Genes and Parvalbumin During Development of Mouse Cortical Neurons.Molecular neurobiology · 2025Article
- Steroid myopathy and rehabilitation in patients with cancer.PM & R : the journal of injury, function, and rehabilitation · 2024Review
- Influence of Frequent Corticosteroid Local Injections on the Expression of Genes and Proteins Related to Fatty Infiltration, Muscle Atrophy, Inflammation, and Fibrosis in Patients With Chronic Rotator Cuff Tears: A Pilot Study.Orthopaedic journal of sports medicine · 2024Article
- Sarcopenic obesity in older adults: a clinical overview.Nature reviews. Endocrinology · 2024Review
- Occurrence of proliferative myositis after COVID-19 vaccination: A case report.Radiology case reports · 2023Article
- Myostatin-mediated regulation of skeletal muscle damage post-acute Aeromonas hydrophila infection in Nile tilapia (Oreochromis niloticus L.).Fish physiology and biochemistry · 2023Article
- Impaired muscle stem cell function and abnormal myogenesis in acquired myopathies.Bioscience reports · 2023Review
- Article
- Balanced Free Essential Amino Acids and Resistance Exercise Training Synergistically Improve Dexamethasone-Induced Impairments in Muscle Strength, Endurance, and Insulin Sensitivity in Mice.International journal of molecular sciences · 2022Article
- Inflammatory myopathy occurring shortly after severe acute respiratory syndrome coronavirus 2 vaccination: two case reports.Journal of medical case reports · 2022Article
- The Role of Autophagy in Skeletal Muscle Diseases.Frontiers in physiology · 2021Review
- Detecting the Effects of the Glucocorticoid Dexamethasone on Primary Human Skeletal Muscle Cells-Differences to the Murine Cell Line.International journal of molecular sciences · 2020Article
- Dexamethasone-induced impairment of post-injury skeletal muscle regeneration.BMC veterinary research · 2019Article
- An unusual case of shortness of breath.Endocrinology, diabetes & metabolism case reports · 2018Article
- Long-Term Dexamethasone Exposure Down-Regulates Hepatic TFR1 and Reduces Liver Iron Concentration in Rats.Nutrients · 2017Article
- Precocious glucocorticoid exposure reduces skeletal muscle satellite cells in the fetal rat.The Journal of endocrinology · 2017Article
- Clinical Relevance of Steroid Use in Neuro-Oncology.Current neurology and neuroscience reports · 2017Review
- Transforming growth factor-β-activated kinase 1 resistance limits glucocorticoid responsiveness to Toll-like receptor 4-mediated inflammation.Immunology · 2015Article
- Isoform-specific SCF(Fbw7) ubiquitination mediates differential regulation of PGC-1α.Journal of cellular physiology · 2015Article
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Accelerated protein degradation via the ubiquitin-proteasome pathway is the principal cause of skeletal muscle wasting associated with common human disease states and pharmacological treatment with glucocorticoids. Although many protein regulatory factors essential for muscle development and regeneration are degraded via the ubiquitin system, little is known about the mechanisms and regulation of this pathway that promote wasting muscle. Here, we demonstrate that, in differentiated myotubes, glucocorticoid, via the glucocorticoid receptor, selectively induces a decrease in protein abundance of MyoD, a master switch for muscle development and regeneration, but not that of its negative regulator Id1. This decrease in MyoD protein results from accelerated degradation after glucocorticoid exposure. Using MyoD and Id1 mutants deficient in either N terminus-dependent or internal lysine-dependent ubiquitination, we further show that these ubiquitination pathways of MyoD degradation are regulated differently from those of Id1 degradation. Specifically, glucocorticoid activates the N-terminal ubiquitination pathway in MyoD degradation in myotubes, without concomitant effects on Id1 degradation. This effect of glucocorticoid on MyoD and Id1 protein degradation is associated with the distinct cellular compartments in which their degradation occurs. Taken together, these results support a key role for the N terminus-dependent ubiquitination pathway in the physiology of muscle protein degradation.
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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.