ArticleJournal of cachexia, sarcopenia and muscle2018
A muscle-specific MuRF1-E2 network requires stabilization of MuRF1-E2 complexes by telethonin, a newly identified substrate.
Article in Journal of cachexia, sarcopenia and muscle, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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Who cites it
32 citing papers in PubMed, 48 citations in OpenAlex.
- Ubiquitin Ligases in pro-atrophic and antiatrophic signaling cascades in muscles.Molecular biology reports · 2026Review
- Combating muscle atrophy: emerging therapeutic targets that are fiber-type-specific.The FEBS journal · 2025Review
- TRIM63/IRF-8 axis promotes tumor progression and immunosuppression of melanoma with BRAF mutation.Cell death & disease · 2025Article
- Glucocorticoid-Mediated Skeletal Muscle Atrophy: Molecular Mechanisms and Potential Therapeutic Targets.International journal of molecular sciences · 2025Review
- Structure predictions of MuRF1-UBE2 complexes identify amino acid residues governing interaction selectivity for each MuRF1-E2 pair.The FEBS journal · 2025Article
- Knockout of the Muscle-Specific E3 Ligase MuRF1 Affects Liver Lipid Metabolism upon Dexamethasone Treatment in Mice.ACS omega · 2024Article
- Targeting MuRF1 to Combat Skeletal Muscle Wasting in Cardiac Cachexia: Mechanisms and Therapeutic Prospects.Medical science monitor : international medical journal of experimental and clinical research · 2024Review
- Uncovering the mechanisms of MuRF1-induced ubiquitylation and revealing similarities with MuRF2 and MuRF3.Biochemistry and biophysics reports · 2024Article
- 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
- Rice OsUBR7 modulates plant height by regulating histone H2B monoubiquitination and cell proliferation.Plant communications · 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
- Case Report: Two New Cases of Autosomal-Recessive Hypertrophic Cardiomyopathy Associated WithFrontiers in genetics · 2022Article
- Hidden Agenda - The Involvement of Endoplasmic Reticulum Stress and Unfolded Protein Response in Inflammation-Induced Muscle Wasting.Frontiers in immunology · 2022Review
- UBE2L3, a Partner of MuRF1/TRIM63, Is Involved in the Degradation of Myofibrillar Actin and Myosin.Cells · 2021Article
- Novel insights into sarcomere regulatory systems control of cardiac thin filament activation.The Journal of general physiology · 2021Article
- Mechanosignaling pathways alter muscle structure and function by post-translational modification of existing sarcomeric proteins to optimize energy usage.Journal of muscle research and cell motility · 2021Article
- Regulation of Glucose Metabolism by MuRF1 and Treatment of Myopathy in Diabetic Mice with Small Molecules Targeting MuRF1.International journal of molecular sciences · 2021Article
- Ubiquitin Ligases at the Heart of Skeletal Muscle Atrophy Control.Molecules (Basel, Switzerland) · 2021Review
- Identification of the MuRF1 Skeletal Muscle Ubiquitylome Through Quantitative Proteomics.Function (Oxford, England) · 2021Article
- Phosphorylation at Serines 157 and 161 Is Necessary for Preserving Cardiac Expression Level and Functions of Sarcomeric Z-Disc Protein Telethonin.Frontiers in physiology · 2021Article
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Authors and funding
11 authors at 5 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundMuscle wasting is observed in the course of many diseases and also during physiological conditions (disuse, ageing). Skeletal muscle mass is largely controlled by the ubiquitin-proteasome system and thus by the ubiquitinating enzymes (E2s and E3s) that target substrates for subsequent degradation. MuRF1 is the only E3 ubiquitin ligase known to target contractile proteins (α-actin, myosins) during catabolic situations. However, MuRF1 depends on E2 ubiquitin-conjugating enzymes for ubiquitin chain formation on the substrates. MuRF1-E2 couples are therefore putative targets for preventing muscle wasting.
methodsWe focused on 14 E2 enzymes that are either expressed in skeletal muscle or up-regulated during atrophying conditions. In this work, we demonstrated that only highly sensitive and complementary interactomic approaches (surface plasmon resonance, yeast three-hybrid, and split green fluorescent protein) allowed the identification of MuRF1 E2 partners.
resultsFive E2 enzymes physically interacted with MuRF1, namely, E2E1, E2G1, E2J1, E2J2, and E2L3. Moreover, we demonstrated that MuRF1-E2E1 and MuRF1-E2J1 interactions are facilitated by telethonin, a newly identified MuRF1 substrate. We next showed that the five identified E2s functionally interacted with MuRF1 since, in contrast to the non-interacting E2D2, their co-expression in HEK293T cells with MuRF1 led to increased telethonin degradation. Finally, we showed that telethonin governed the affinity between MuRF1 and E2E1 or E2J1.
conclusionsWe report here the first MuRF1-E2s network, which may prove valuable for deciphering the precise mechanisms involved in the atrophying muscle programme and for proposing new therapeutical approaches.
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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.