ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2001
Src, Fyn, and Yes are not required for neuromuscular synapse formation but are necessary for stabilization of agrin-induced clusters of acetylcholine receptors.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
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Who cites it
37 citing papers in PubMed, 100 citations in OpenAlex.
- High-content image-based pooled screens reveal regulators of synaptogenesis.Cell reports · 2025Article
- Protein networking: nicotinic acetylcholine receptors and their protein-protein-associations.Molecular and cellular biochemistry · 2024Review
- Article
- 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
- Article
- The Neuromuscular Junction in Health and Disease: Molecular Mechanisms Governing Synaptic Formation and Homeostasis.Frontiers in molecular neuroscience · 2020Review
- Muscle-Specific Kinase Myasthenia Gravis.Frontiers in immunology · 2020Review
- Vezatin is required for the maturation of the neuromuscular synapse.Molecular biology of the cell · 2019Article
- MACF1 links Rapsyn to microtubule- and actin-binding proteins to maintain neuromuscular synapses.The Journal of cell biology · 2019Article
- Fundamental Molecules and Mechanisms for Forming and Maintaining Neuromuscular Synapses.International journal of molecular sciences · 2018Review
- Beta-2 Adrenergic Receptor Agonists Enhance AChR Clustering in C2C12 Myotubes: Implications for Therapy of Myasthenic Disorders.Journal of neuromuscular diseases · 2018Article
- Diverging roles for Lrp4 and Wnt signaling in neuromuscular synapse development during evolution.Genes & development · 2016Article
- Α-Dystrobrevin-1 recruits Grb2 and α-catulin to organize neurotransmitter receptors at the neuromuscular junction.Journal of cell science · 2016Article
- Forced expression of muscle specific kinase slows postsynaptic acetylcholine receptor loss in a mouse model of MuSK myasthenia gravis.Physiological reports · 2015Article
- Mechanisms controlling neuromuscular junction stability.Cellular and molecular life sciences : CMLS · 2015Review
- Biglycan is an extracellular MuSK binding protein important for synapse stability.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2012Article
- Role of extracellular matrix proteins and their receptors in the development of the vertebrate neuromuscular junction.Developmental neurobiology · 2011Review
- To build a synapse: signaling pathways in neuromuscular junction assembly.Development (Cambridge, England) · 2010Review
- The function of cortactin in the clustering of acetylcholine receptors at the vertebrate neuromuscular junction.PloS one · 2009Article
- The function of Shp2 tyrosine phosphatase in the dispersal of acetylcholine receptor clusters.BMC neuroscience · 2008Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
Abstract
Mice deficient in src and fyn or src and yes move and breathe poorly and die perinatally, consistent with defects in neuromuscular function. Src and Fyn are associated with acetylcholine receptors (AChRs) in muscle cells, and Src and Yes can act downstream of ErbB2, suggesting roles for Src family kinases in signaling pathways regulating neuromuscular synapse formation. We studied neuromuscular synapses in src(-/-); fyn(-/-) and src(-/-); yes(-/-) mutant mice and found that muscle development, motor axon pathfinding, clustering of postsynaptic proteins, and synapse-specific transcription are normal in these double mutants, showing that these pairs of kinases are not required for early steps in synapse formation. We generated muscle cell lines lacking src and fyn and found that neural agrin and laminin-1 induced normal clustering of AChRs and that agrin induced normal tyrosine phosphorylation of the AChR beta subunit in the absence of Src and Fyn. Another Src family member, most likely Yes, was associated with AChRs and phosphorylated by agrin in myotubes lacking Src and Fyn, indicating that Yes may compensate for the loss of Src and Fyn. Nevertheless, PP1 and PP2, inhibitors of Src-class kinases, did not inhibit agrin signaling, suggesting that Src class kinase activity is dispensable for agrin-induced clustering and tyrosine phosphorylation of AChRs. AChR clusters, however, were less stable in myotubes lacking Src and Fyn but not in PP1- or PP2-treated wild-type cells. These data show that the stabilization of agrin-induced AChR clusters requires Src and Fyn and suggest that the adaptor activities, rather than the kinase activities, of these kinases are essential for this stabilization.
Indexed as
Identifiers
11312300PMC6762551W2114892569What OpenQuestion holds
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.