ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2012
Biglycan is an extracellular MuSK binding protein important for synapse stability.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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Who cites it
33 citing papers in PubMed, 67 citations in OpenAlex.
- MuSK IgG4 autoantibodies cause myasthenia gravis by inhibiting binding between MuSK and Lrp4.Proceedings of the National Academy of Sciences of the United States of America · 2013Trial
- Muscle-Specific Kinase Signaling and Its Therapeutic Potential.Muscle & nerve · 2026Review
- The MuSK-BMP pathway maintains myofiber size in slow muscle through regulation of Akt-mTOR signaling.Skeletal muscle · 2024Article
- Microscopic and Biochemical Hallmarks ofInternational journal of molecular sciences · 2023Article
- NMJ-related diseases beyond the congenital myasthenic syndromes.Frontiers in cell and developmental biology · 2023Review
- Post-synaptic specialization of the neuromuscular junction: junctional folds formation, function, and disorders.Cell & bioscience · 2022Review
- Temporal changes in the muscle extracellular matrix due to volumetric muscle loss injury.Connective tissue research · 2022Article
- Contribution of extracellular matrix components to the stiffness of skeletal muscle contractures in patients with cerebral palsy.Connective tissue research · 2021Article
- Secreted Signaling Molecules at the Neuromuscular Junction in Physiology and Pathology.International journal of molecular sciences · 2021Review
- Neural Tissue Homeostasis and Repair Is Regulated via CS and DS Proteoglycan Motifs.Frontiers in cell and developmental biology · 2021Review
- Secretome Analysis of Inductive Signals for BM-MSC Transdifferentiation into Salivary Gland Progenitors.International journal of molecular sciences · 2020Article
- Multiple MuSK signaling pathways and the aging neuromuscular junction.Neuroscience letters · 2020Review
- AChR β-Subunit mRNAs Are Stabilized by HuR in a Mouse Model of Congenital Myasthenic Syndrome With Acetylcholinesterase Deficiency.Frontiers in molecular neuroscience · 2020Article
- Myasthenia Gravis: From the Viewpoint of Pathogenicity Focusing on Acetylcholine Receptor Clustering, Trans-Synaptic Homeostasis and Synaptic Stability.Frontiers in molecular neuroscience · 2020Article
- Non-Glycanated Biglycan and LTBP4: Leveraging the extracellular matrix for Duchenne Muscular Dystrophy therapeutics.Matrix biology : journal of the International Society for Matrix Biology · 2018Review
- Synaptic Homeostasis and Its Immunological Disturbance in Neuromuscular Junction Disorders.International journal of molecular sciences · 2017Review
- Contaminants in commercial preparations of 'purified' small leucine-rich proteoglycans may distort mechanistic studies.Bioscience reports · 2017Article
- MuSK is a BMP co-receptor that shapes BMP responses and calcium signaling in muscle cells.Science signaling · 2016Article
- Collagen Q and anti-MuSK autoantibody competitively suppress agrin/LRP4/MuSK signaling.Scientific reports · 2015Article
- Galectin-1 Protein Therapy Prevents Pathology and Improves Muscle Function in the mdx Mouse Model of Duchenne Muscular Dystrophy.Molecular therapy : the journal of the American Society of Gene Therapy · 2015Article
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Authors and funding
16 authors at 7 institutions in 1 country.
Funding
Abstract
The receptor tyrosine kinase MuSK is indispensable for nerve-muscle synapse formation and maintenance. MuSK is necessary for prepatterning of the endplate zone anlage and as a signaling receptor for agrin-mediated postsynaptic differentiation. MuSK-associated proteins such as Dok7, LRP4, and Wnt11r are involved in these early events in neuromuscular junction formation. However, the mechanisms regulating synapse stability are poorly understood. Here we examine a novel role for the extracellular matrix protein biglycan in synapse stability. Synaptic development in fetal and early postnatal biglycan null (bgn(-/o)) muscle is indistinguishable from wild-type controls. However, by 5 weeks after birth, nerve-muscle synapses in bgn(-/o) mice are abnormal as judged by the presence of perijunctional folds, increased segmentation, and focal misalignment of acetylcholinesterase and AChRs. These observations indicate that previously occupied presynaptic and postsynaptic territory has been vacated. Biglycan binds MuSK and the levels of this receptor tyrosine kinase are selectively reduced at bgn(-/o) synapses. In bgn(-/o) myotubes, the initial stages of agrin-induced MuSK phosphorylation and AChR clustering are normal, but the AChR clusters are unstable. This stability defect can be substantially rescued by the addition of purified biglycan. Together, these results indicate that biglycan is an extracellular ligand for MuSK that is important for synapse stability.
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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.