ArticleScience signaling2018
A DGKζ-FoxO-ubiquitin proteolytic axis controls fiber size during skeletal muscle remodeling.
Article in Science signaling, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 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.
The trial behind it
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Who cites it
33 citing papers in PubMed, 51 citations in OpenAlex.
- Transient MYC Mimicking the Exercise Response Orchestrates Multifaceted Skeletal Muscle Adaptations.bioRxiv : the preprint server for biology · 2026Article
- Response of UBR-box E3 ubiquitin ligases and protein quality control pathways to perturbations in protein synthesis and skeletal muscle size.American journal of physiology. Cell physiology · 2025Article
- DGKs in lipid signaling and disease intervention: structural basis, pathological mechanisms, and emerging therapeutic strategies.Cellular & molecular biology letters · 2025Review
- Response of UBR-box E3 ubiquitin ligases and protein quality control pathways to perturbations in protein synthesis and skeletal muscle size.bioRxiv : the preprint server for biology · 2025Article
- UBR5: A New Player in Protein Quality Control for Skeletal Muscle Growth and Remodeling.Exercise and sport sciences reviews · 2025Review
- Resistance exercise and skeletal muscle: protein synthesis, degradation, and controversies.European journal of applied physiology · 2025Review
- Key genes and processes affected by atorvastatin treatment in mouse diaphragm muscle.Archives of toxicology · 2025Article
- Functions and Therapeutic Potentials of Long Noncoding RNA in Skeletal Muscle Atrophy and Dystrophy.Journal of cachexia, sarcopenia and muscle · 2025Review
- Role of PI3 Kinases in Cell Signaling and Soleus Muscle Atrophy During Three Days of Unloading.International journal of molecular sciences · 2025Article
- Dual roles of mTOR in skeletal muscle adaptation: coordinating hypertrophic and mitochondrial biogenesis pathways for exercise-induced chronic disease management.Frontiers in medicine · 2025Article
- Diacylglycerol kinase δ is required for skeletal muscle development and regeneration.FASEB bioAdvances · 2025Article
- Review
- 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
- Mechanisms of mechanical overload-induced skeletal muscle hypertrophy: current understanding and future directions.Physiological reviews · 2023Review
- The emerging role of Piezo1 channels in skeletal muscle physiology.Biophysical reviews · 2023Review
- Exercise metabolism and adaptation in skeletal muscle.Nature reviews. Molecular cell biology · 2023Review
- RhoA/ROCK signalling activated by ARHGEF3 promotes muscle weakness via autophagy in dystrophic mdx mice.Journal of cachexia, sarcopenia and muscle · 2023Article
- A novel method for visualizingiScience · 2023Article
- Alcohol, Resistance Exercise, and mTOR Pathway Signaling: An Evidence-Based Narrative Review.Biomolecules · 2022Review
- CORP: Gene delivery into murine skeletal muscle using in vivo electroporation.Journal of applied physiology (Bethesda, Md. : 1985) · 2022Review
Corrections and comments
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Authors and funding
7 authors at 1 institution in 2 countries.
Funding
Abstract
Skeletal muscle rapidly remodels in response to various stresses, and the resulting changes in muscle mass profoundly influence our health and quality of life. We identified a diacylglycerol kinase ζ (DGKζ)-mediated pathway that regulated muscle mass during remodeling. During mechanical overload, DGKζ abundance was increased and required for effective hypertrophy. DGKζ not only augmented anabolic responses but also suppressed ubiquitin-proteasome system (UPS)-dependent proteolysis. We found that DGKζ inhibited the transcription factor FoxO that promotes the induction of the UPS. This function was mediated through a mechanism that was independent of kinase activity but dependent on the nuclear localization of DGKζ. During denervation, DGKζ abundance was also increased and was required for mitigating the activation of FoxO-UPS and the induction of atrophy. Conversely, overexpression of DGKζ prevented fasting-induced atrophy. Therefore, DGKζ is an inhibitor of the FoxO-UPS pathway, and interventions that increase its abundance could prevent 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.