ArticleAge (Dordrecht, Netherlands)2013
Regulation of nicotinic acetylcholine receptor turnover by MuRF1 connects muscle activity to endo/lysosomal and atrophy pathways.
Article in Age (Dordrecht, Netherlands), 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.
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Who cites it
47 citing papers in PubMed, 64 citations in OpenAlex.
- Neuromuscular junctions are stable in patients with cancer cachexia.The Journal of clinical investigation · 2020Trial
- Presynaptic compensation sustains neuromuscular transmission in the mouse diaphragm at a late stage of aging.Biogerontology · 2026Article
- The miR-206-3p/Cpeb1 axis delays acetylcholine receptor degradation and preserves neuromuscular junction stability in denervation-induced muscle atrophy.Cellular and molecular life sciences : CMLS · 2026Article
- Article
- Sympathetic innervation in skeletal muscle and its role at the neuromuscular junction.Journal of muscle research and cell motility · 2024Review
- Regeneration of neuromuscular synapses after acute and chronic denervation by inhibiting the gerozyme 15-prostaglandin dehydrogenase.Science translational medicine · 2023Article
- Direct electrical stimulation impacts on neuromuscular junction morphology on both stimulated and unstimulated contralateral soleus.Journal of cachexia, sarcopenia and muscle · 2023Article
- Molecular mechanisms of post-burn muscle wasting and the therapeutic potential of physical exercise.Journal of cachexia, sarcopenia and muscle · 2023Review
- Targeting Mitochondria and Oxidative Stress in Cancer- and Chemotherapy-Induced Muscle Wasting.Antioxidants & redox signaling · 2023Review
- Age-Related Dysfunction in Proteostasis and Cellular Quality Control in the Development of Sarcopenia.Cells · 2023Review
- Ubiquitin Ligases in Longevity and Aging Skeletal Muscle.International journal of molecular sciences · 2022Review
- CORP: Gene delivery into murine skeletal muscle using in vivo electroporation.Journal of applied physiology (Bethesda, Md. : 1985) · 2022Review
- Skeletal muscle sympathetic denervation disrupts the neuromuscular junction postterminal organization: A single-cell quantitative approach.Molecular and cellular neurosciences · 2022Article
- Supraphysiological activation of TAK1 promotes skeletal muscle growth and mitigates neurogenic atrophy.Nature communications · 2022Article
- KMT5B is required for early motor development.Frontiers in genetics · 2022Article
- Long-term, induced expression of Hand2 in peripheral sympathetic neurons ameliorates sarcopenia in geriatric mice.Journal of cachexia, sarcopenia and muscle · 2021Article
- The emerging role of the sympathetic nervous system in skeletal muscle motor innervation and sarcopenia.Ageing research reviews · 2021Review
- The Metabolic Stability of the Nicotinic Acetylcholine Receptor at the Neuromuscular Junction.Cells · 2021Review
- Heart and neural crest derivative 2-induced preservation of sympathetic neurons attenuates sarcopenia with aging.Journal of cachexia, sarcopenia and muscle · 2021Article
- Ubiquitin Ligases at the Heart of Skeletal Muscle Atrophy Control.Molecules (Basel, Switzerland) · 2021Review
Corrections and comments
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Authors and funding
11 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Muscle atrophy is a process of muscle wasting induced under a series of catabolic stress conditions, such as denervation, disuse, cancer cachexia, heart and renal failure, AIDS, and aging. Neuromuscular junctions (NMJs), the synapses between motor neurons and muscle fibers undergo major changes in atrophying muscles, ranging from mild morphological alterations to complete disintegration. In this study, we hypothesized that remodeling of NMJs and muscle atrophy could be linked together. To test this, we examined if a major atrophy-promoting E3 ubiquitin ligase, MuRF1, is involved in the maintenance of NMJs. Immunofluorescence revealed that MuRF1 is highly enriched close to the NMJ. Affinity precipitation and in vivo imaging showed that MuRF1 interacts in endocytic structures with both, acetylcholine receptor, the primary postsynaptic protein of the NMJ, as well as with Bif-1, an autophagy- and endocytosis-regulating factor. In vivo imaging, radio labeling, and weighing approaches demonstrated that metabolic destabilization of acetylcholine receptors and muscle atrophy induced by denervation were significantly rescued in MuRF1-KO animals. Notably, interaction with Bif-1, and the rescue of AChR lifetime and muscle atrophy were specific to MuRF1 but not MuRF2. Our data demonstrate an involvement of MuRF1 in membrane protein-turnover, including the degradation of AChRs at the NMJ under atrophying conditions where MuRF1 also interacts and associates with Bif-1.
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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.