ArticleLife sciences2019
UCHL1 regulates muscle fibers and mTORC1 activity in skeletal muscle.
Article in Life sciences, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 22 citations in OpenAlex.
- Deubiquitinase YOD1 Inhibition Suppresses DEX- and Denervation-Induced Muscle Atrophy Through MAFbx Destabilization.Journal of cachexia, sarcopenia and muscle · 2026Article
- UCHL1 enhancesHistology and histopathology · 2026Article
- AMPK/mTOR balance during exercise: implications for insulin resistance in aging muscle.Molecular and cellular biochemistry · 2025Review
- Article
- Skeletal Muscle UCHL1 Negatively Regulates Muscle Development and Recovery after Muscle Injury.International journal of molecular sciences · 2024Article
- Article
- Human myofiber-enriched aging-induced lncRNA FRAIL1 promotes loss of skeletal muscle function.Aging cell · 2024Article
- Integrated 4D Analysis of Intramuscular Fat Deposition: Quantitative Proteomic and Transcriptomic Studies in Wannanhua Pig Longissimus Dorsi Muscle.Animals : an open access journal from MDPI · 2024Article
- Pivotal Role of Ubiquitin Carboxyl-Terminal Hydrolase L1 (UCHL1) in Uterine Leiomyoma.Biomolecules · 2023Article
- The deubiquitinase UCHL1 negatively controls osteoclastogenesis by regulating TAZ/NFATC1 signalling.International journal of biological sciences · 2023Article
- UCHL1 Regulates Lipid and Perilipin 2 Level in Skeletal Muscle.Frontiers in physiology · 2022Article
- Ubiquitin Carboxyl-Terminal Hydrolase L1 of Cardiomyocytes Promotes Macroautophagy and Proteostasis and Protects Against Post-myocardial Infarction Cardiac Remodeling and Heart Failure.Frontiers in cardiovascular medicine · 2022Article
- Enhanced pro-BDNF-p75NTR pathway activity in denervated skeletal muscle.Life sciences · 2021Article
- A novel c.-652C>T mutation in UCHL1 gene is associated with the growth performance in Yangzhou goose.Poultry science · 2021Article
- Blockage of UCHL1 activity attenuates cardiac remodeling in spontaneously hypertensive rats.Hypertension research : official journal of the Japanese Society of Hypertension · 2020Article
- UCHL1 regulates oxidative activity in skeletal muscle.PloS one · 2020Article
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
aimsSkeletal muscle wasting is associated with many chronic diseases. Effective prevention and treatment of muscle wasting remain as a challenging task due to incomplete understanding of mechanisms by which muscle mass is maintained and regulated. This study investigated the functional role of Ubiquitin C-terminal hydrolase L1 (UCHL1) in skeletal muscle. MAIN
methodsMice with skeletal muscle specific gene knockout of UCHL1 and C2C12 myoblast cells with UCHL1 knockdown were used. Muscle fiber types and size were measured using tissue or cell staining. The mammalian target of rapamycin complex 1 (mTORC1) and mTORC2 activities were assessed with the phosphorylation of their downstream targets. KEY
findingsIn mouse skeletal muscle, UCHL1 was primarily expressed in slow twitch muscle fibers. Mice with skeletal muscle specific knockout (skmKO) of UCHL1 exhibited enlarged muscle fiber sizes in slow twitch soleus but not fast twitch extensor digitorum longus (EDL) muscle. Meanwhile, UCHL1 skmKO enhanced mTORC1 activity and reduced mTORC2 activity in soleus but not in EDL. Consistently, in C2C12 cells, UCHL1 knockdown increased the myotube size, enhanced mTORC1 activity, and reduced mTORC2 activities as compared with control cells. UCHL1 knockdown did not change the major proteins of mTOR complex but decreased the protein turnover of PRAS40, an inhibitory factor of mTORC1. SIGNIFICANCE: These data revealed a novel function of UCHL1 in regulation of mTORC1 activity and skeletal muscle growth in slow twitch skeletal muscle. Given the upregulation of UCHL1 in denervation and spinal muscle atrophy, our finding advances understanding of regulators that are involved in muscle wasting.
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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.