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Regulation of miR-206 in denervated and dystrophic muscles, and its effect on acetylcholine receptor clustering.
J Cell Sci
December 2024
Department of Molecular, Cellular and Developmental Biology, 1105 N. University Avenue, Ann Arbor, MI 48109, USA.
The muscle-specific microRNA miR-206 has recently emerged as a potential regulator of genes involved in the formation and regeneration of the neuromuscular junction (NMJ). This study investigated miR-206-3p (miR-206) expression in synaptic and non-synaptic regions of denervated mice and α-dystrobrevin (Dtna)-knockout mice, as well as its impact on the formation and/or maintenance of agrin-induced acetylcholine receptor (AChR) clusters. In denervated, Dtna-deficient and crushed muscles, miR-206 expression significantly increased compared to what was seen for innervated muscles.
View Article and Find Full Text PDFNeuromuscular Regeneration of Volumetric Muscle Loss Injury in Response to Agrin-Functionalized Tissue Engineered Muscle Grafts and Rehabilitative Exercise.
Adv Healthc Mater
January 2025
Translational Tissue Engineering Center, School of Medicine, Johns Hopkins University, Baltimore, MD, 21231, USA.
Neuromuscular deficits compound the loss of contractile tissue in volumetric muscle loss (VML). Two avenues for promoting recovery are neuromuscular junction (NMJ)-promoting substrates (e.g.
View Article and Find Full Text PDFIgG1-3 MuSK Antibodies Inhibit AChR Cluster Formation, Restored by SHP2 Inhibitor, Despite Normal MuSK, DOK7, or AChR Subunit Phosphorylation.
Neurol Neuroimmunol Neuroinflamm
November 2023
From the Nuffield Department of Clinical Neurosciences (M.C., W.W.L., S.M., R.W., D.B., J.A.C., A.V.), University of Oxford; Norfolk and Norwich University Hospital (M.C.); The Walton Centre NHS Foundation Trust (S.H.), Liverpool, United Kingdom; and Department of Neuroscience (A.E.), Catholic University, Rome, Italy.
Background And Objectives: Up to 50% of patients with myasthenia gravis (MG) without acetylcholine receptor antibodies (AChR-Abs) have antibodies to muscle-specific kinase (MuSK). Most MuSK antibodies (MuSK-Abs) are IgG4 and inhibit agrin-induced MuSK phosphorylation, leading to impaired clustering of AChRs at the developing or mature neuromuscular junction. However, IgG1-3 MuSK-Abs also exist in MuSK-MG patients, and their potential mechanisms have not been explored fully.
View Article and Find Full Text PDFThe collagen ColQ binds to LRP4 and regulates the activation of the Muscle-Specific Kinase-LRP4 receptor complex by agrin at the neuromuscular junction.
J Biol Chem
August 2023
Université Paris Cité, CNRS, Saints-Pères Paris Institute for the Neurosciences, Paris, France. Electronic address:
Collagen Q (ColQ) is a nonfibrillar collagen that plays a crucial role at the vertebrate neuromuscular junction (NMJ) by anchoring acetylcholinesterase to the synapse. ColQ also functions in signaling, as it regulates acetylcholine receptor clustering and synaptic gene expression, in a manner dependent on muscle-specific kinase (MuSK), a key protein in NMJ formation and maintenance. MuSK forms a complex with low-density lipoprotein receptor-related protein 4 (LRP4), its coreceptor for the proteoglycan agrin at the NMJ.
View Article and Find Full Text PDFNerve-independent formation of membrane infoldings at topologically complex postsynaptic apparatus by caveolin-3.
Sci Adv
June 2023
School of Biomedical Sciences, Li Ka Shing Faculty of Medicine, The University of Hong Kong, Hong Kong, China.
Junctional folds are unique membrane specializations developed progressively during the postnatal maturation of vertebrate neuromuscular junctions (NMJs), but how they are formed remains elusive. Previous studies suggested that topologically complex acetylcholine receptor (AChR) clusters in muscle cultures undergo a series of transformations, resembling the postnatal maturation of NMJs in vivo. We first demonstrated the presence of membrane infoldings at AChR clusters in cultured muscles.
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