ArticleJournal of cell science2017
Spatial distribution and molecular dynamics of dystrophin glycoprotein components at the neuromuscular junction
Article in Journal of cell science, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 15 citations in OpenAlex.
- Cytoplasmic region of beta-dystroglycan is essential for postsynaptic maturation and neuromuscular function in mice.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Optical coherence tomography findings in Duchenne muscular dystrophy.BMC ophthalmology · 2026Article
- Sirt6 Mono-ADP-Ribosylates YY1 to Promote Dystrophin Expression for Neuromuscular Transmission.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- The role of Rapsyn in neuromuscular junction and congenital myasthenic syndrome.Biomolecules & biomedicine · 2023Review
- Distinct roles of the dystrophin-glycoprotein complex: α-dystrobrevin and α-syntrophin in the maintenance of the postsynaptic apparatus of the neuromuscular synapse.Human molecular genetics · 2022Article
- Defects of full-length dystrophin trigger retinal neuron damage and synapse alterations by disrupting functional autophagy.Cellular and molecular life sciences : CMLS · 2021Article
- The role of the dystrophin glycoprotein complex on the neuromuscular system.Neuroscience letters · 2020Review
- Arhgef5 Binds α-Dystrobrevin 1 and Regulates Neuromuscular Junction Integrity.Frontiers in molecular neuroscience · 2020Article
- Utrophin up-regulation by artificial transcription factors induces muscle rescue and impacts the neuromuscular junction in mdx mice.Biochimica et biophysica acta. Molecular basis of disease · 2018Article
- Liprin-α-1 is a novel component of the murine neuromuscular junction and is involved in the organization of the postsynaptic machinery.Scientific reports · 2017Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 2 countries.
Funding
Abstract
A bimolecular fluorescence complementation (BiFC) approach was used to study the molecular interactions between different components of the postsynaptic protein complex at the neuromuscular junction of living mice. We show that rapsyn forms complex with both α-dystrobrevin and α-syntrophin at the crests of junctional folds. The linkage of rapsyn to α-syntrophin and/or α-dystrobrevin is mediated by utrophin, a protein localized at acetylcholine receptor (AChR)-rich domains. In mice deficient in α-syntrophin, in which utrophin is no longer present at the synapse, rapsyn interaction with α-dystrobrevin was completely abolished. This interaction was completely restored when either utrophin or α-syntrophin was introduced into muscles deficient in α-syntrophin. However, in neuromuscular junctions deficient in α-dystrobrevin, in which utrophin is retained, complex formation between rapsyn and α-syntrophin was unaffected. Using fluorescence recovery after photobleaching, we found that α-syntrophin turnover is 5-7 times faster than that of AChRs, and loss of α-dystrobrevin has no effect on rapsyn and α-syntrophin half-life, whereas the half-life of AChR was significantly altered. Altogether, these results provide new insights into the spatial distribution of dystrophin glycoprotein components and their dynamics in living mice.
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