ArticleJournal of cachexia, sarcopenia and muscle2016
Muscle RING-finger 2 and 3 maintain striated-muscle structure and function.
Article in Journal of cachexia, sarcopenia and muscle, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 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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Who cites it
31 citing papers in PubMed, 51 citations in OpenAlex.
- The hallmarks of skeletal muscle health.Nature metabolism · 2026Review
- The Novel MuRF2 Target SNX5 Regulates PKA Activity Through Stabilization of RI-α and Controls Myogenic Differentiation.Journal of cachexia, sarcopenia and muscle · 2025Article
- Article
- Differentially co-expressed myofibre transcripts associated with abnormal myofibre proportion in chronic obstructive pulmonary disease.Journal of cachexia, sarcopenia and muscle · 2024Article
- Metabolic remodeling in cardiac hypertrophy and heart failure with reduced ejection fraction occurs independent of transcription factor EB in mice.Frontiers in cardiovascular medicine · 2023Article
- Sarcopenia: Molecular regulatory network for loss of muscle mass and function.Frontiers in nutrition · 2023Review
- The Transcription Factor EB (TFEB) Sensitizes the Heart to Chronic Pressure Overload.International journal of molecular sciences · 2022Article
- Inhibition of the NLRP3/IL-1β axis protects against sepsis-induced cardiomyopathy.Journal of cachexia, sarcopenia and muscle · 2021Article
- Striated muscle proteins are regulated both by mechanical deformation and by chemical post-translational modification.Biophysical reviews · 2021Review
- Out of Control: The Role of the Ubiquitin Proteasome System in Skeletal Muscle during Inflammation.Biomolecules · 2021Review
- The ubiquitin ligase Ozz decreases the replacement rate of embryonic myosin in myofibrils.Physiological reports · 2021Article
- Maintenance of type 2 glycolytic myofibers with age by Mib1-Actn3 axis.Nature communications · 2021Article
- Under construction: The dynamic assembly, maintenance, and degradation of the cardiac sarcomere.Journal of molecular and cellular cardiology · 2020Review
- Emerging Strategies Targeting Catabolic Muscle Stress Relief.International journal of molecular sciences · 2020Review
- Serum amyloid A1 mediates myotube atrophy via Toll-like receptors.Journal of cachexia, sarcopenia and muscle · 2020Article
- Activation of Tripartite Motif Containing 63 Expression by Transcription Factor EB and Transcription Factor Binding to Immunoglobulin Heavy Chain Enhancer 3 Is Regulated by Protein Kinase D and Class IIa Histone Deacetylases.Frontiers in physiology · 2020Article
- Recent developments in the field of cachexia, sarcopenia, and muscle wasting: highlights from the 11th Cachexia Conference.Journal of cachexia, sarcopenia and muscle · 2019Article
- The E3 ligase MuRF2 plays a key role in the functional capacity of skeletal muscle fibroblasts.Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica · 2019Article
- Metabolic disorders in heart failure and cancer.ESC heart failure · 2018Review
- MicroRNAs in muscle wasting.Journal of cachexia, sarcopenia and muscle · 2018Article
Corrections and comments
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Authors and funding
19 authors at 5 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThe Muscle-specific RING-finger (MuRF) protein family of E3 ubiquitin ligases is important for maintenance of muscular structure and function. MuRF proteins mediate adaptation of striated muscles to stress. MuRF2 and MuRF3 bind to microtubules and are implicated in sarcomere formation with noticeable functional redundancy. However, if this redundancy is important for muscle function in vivo is unknown. Our objective was to investigate cooperative function of MuRF2 and MuRF3 in the skeletal muscle and the heart in vivo.
methodsMuRF2 and MuRF3 double knockout mice (DKO) were generated and phenotypically characterized. Skeletal muscle and the heart were investigated by morphological measurements, histological analyses, electron microscopy, immunoblotting, and real-time PCR. Isolated muscles were subjected to in vitro force measurements. Cardiac function was determined by echocardiography and working heart preparations. Function of cardiomyocytes was measured in vitro. Cell culture experiments and mass-spectrometry were used for mechanistic analyses.
resultsDKO mice showed a protein aggregate myopathy in skeletal muscle. Maximal force development was reduced in DKO soleus and extensor digitorum longus. Additionally, a fibre type shift towards slow/type I fibres occurred in DKO soleus and extensor digitorum longus. MuRF2 and MuRF3-deficient hearts showed decreased systolic and diastolic function. Further analyses revealed an increased expression of the myosin heavy chain isoform beta/slow and disturbed calcium handling as potential causes for the phenotype in DKO hearts.
conclusionsThe redundant function of MuRF2 and MuRF3 is important for maintenance of skeletal muscle and cardiac structure and function in vivo.
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