ArticleThe EMBO journal2012
The p97/VCP ATPase is critical in muscle atrophy and the accelerated degradation of muscle proteins.
Article in The EMBO journal, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers.
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Who cites it
58 citing papers in PubMed, 86 citations in OpenAlex.
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- Mitochondrial Maintenance in Skeletal Muscle.Cold Spring Harbor perspectives in biology · 2025Review
- The protein segregase VCP/p97 promotes host antifungal defense via regulation of SYK activation.PLoS pathogens · 2024Article
- Proteasome gene expression is controlled by coordinated functions of multiple transcription factors.The Journal of cell biology · 2024Article
- USP3: Key deubiquitylation enzyme in human diseases.Cancer science · 2024Review
- The RU486-dependent activation of the GeneSwitch system in adult muscles leads to severe adverse effects in Drosophila.G3 (Bethesda, Md.) · 2024Article
- Bidirectional substrate shuttling between the 26S proteasome and the Cdc48 ATPase promotes protein degradation.Molecular cell · 2024Article
- Lysine methylation signaling in skeletal muscle biology: from myogenesis to clinical insights.The Biochemical journal · 2023Review
- A critical discussion on the relationship between E3 ubiquitin ligases, protein degradation, and skeletal muscle wasting: it's not that simple.American journal of physiology. Cell physiology · 2023Review
- MYTHO is a novel regulator of skeletal muscle autophagy and integrity.Nature communications · 2023Article
- The AAA-ATPase ATAD1 and its partners promote degradation of desmin intermediate filaments in muscle.EMBO reports · 2022Article
- Dual roles of mTORC1-dependent activation of the ubiquitin-proteasome system in muscle proteostasis.Communications biology · 2022Article
- The p97-Nploc4 ATPase complex plays a role in muscle atrophy during cancer and amyotrophic lateral sclerosis.Journal of cachexia, sarcopenia and muscle · 2022Article
- Post-meeting report of the 2022 On-site Padua Days on Muscle and Mobility Medicine, March 30 - April 3, 2022, Padua, Italy.European journal of translational myology · 2022Article
- The 2022 On-site Padua Days on Muscle and Mobility Medicine hosts the University of Florida Institute of Myology and the Wellstone Center, March 30 - April 3, 2022 at the University of Padua and Thermae of Euganean Hills, Padua, Italy: The collection of abstracts.European journal of translational myology · 2022Article
- Integration of proteomic and genetic approaches to assess developmental muscle atrophy.The Journal of experimental biology · 2021Article
- Out of Control: The Role of the Ubiquitin Proteasome System in Skeletal Muscle during Inflammation.Biomolecules · 2021Review
- Deletion of muscleJournal of applied physiology (Bethesda, Md. : 1985) · 2021Article
- UBE2L3, a Partner of MuRF1/TRIM63, Is Involved in the Degradation of Myofibrillar Actin and Myosin.Cells · 2021Article
- Proteasome stress in skeletal muscle mounts a long-range protective response that delays retinal and brain aging.Cell metabolism · 2021Article
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
The p97/VCP ATPase complex facilitates the extraction and degradation of ubiquitinated proteins from larger structures. We therefore studied if p97 participates to the rapid degradation of myofibrillar proteins during muscle atrophy. Electroporation of a dominant negative p97 (DNp97), but not the WT, into mouse muscle reduced fibre atrophy caused by denervation and food deprivation. DNp97 (acting as a substrate-trap) became associated with specific myofibrillar proteins and its cofactors, Ufd1 and p47, and caused accumulation of ubiquitinated components of thin and thick filaments, which suggests a role for p97 in extracting ubiquitinated proteins from myofibrils. DNp97 expression in myotubes reduced overall proteolysis by proteasomes and lysosomes and blocked the accelerated proteolysis induced by FoxO3, which is essential for atrophy. Expression of p97, Ufd1 and p47 increases following denervation, at times when myofibrils are rapidly degraded. Surprisingly, p97 inhibition, though toxic to most cells, caused rapid growth of myotubes (without enhancing protein synthesis) and hypertrophy of adult muscles. Thus, p97 restrains post-natal muscle growth, and during atrophy, is essential for the accelerated degradation of most muscle proteins.
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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.