ArticleThe Journal of cell biology1993
Clustering and immobilization of acetylcholine receptors by the 43-kD protein: a possible role for dystrophin-related protein.
Article in The Journal of cell biology, 1993. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 106 citations in OpenAlex.
- Motor function recovery: deciphering a regenerative niche at the neuromuscular synapse.Biological reviews of the Cambridge Philosophical Society · 2021Review
- The role of the dystrophin glycoprotein complex on the neuromuscular system.Neuroscience letters · 2020Review
- Forced expression of muscle specific kinase slows postsynaptic acetylcholine receptor loss in a mouse model of MuSK myasthenia gravis.Physiological reports · 2015Article
- Muscle-specific kinase (MuSK) autoantibodies suppress the MuSK pathway and ACh receptor retention at the mouse neuromuscular junction.The Journal of physiology · 2014Article
- Rapsyn interacts with the muscle acetylcholine receptor via alpha-helical domains in the alpha, beta, and epsilon subunit intracellular loops.Neuroscience · 2009Article
- Rapsyn carboxyl terminal domains mediate muscle specific kinase-induced phosphorylation of the muscle acetylcholine receptor.Neuroscience · 2008Article
- Modulation of utrophin A mRNA stability in fast versus slow muscles via an AU-rich element and calcineurin signaling.Nucleic acids research · 2008Article
- Differential requirement for MuSK and dystroglycan in generating patterns of neuromuscular innervation.Proceedings of the National Academy of Sciences of the United States of America · 2007Article
- The role of the cytoskeleton in neuromuscular junction formation.Journal of molecular neuroscience : MN · 2006Article
- A role for the juxtamembrane domain of beta-dystroglycan in agrin-induced acetylcholine receptor clustering.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2003Article
- Src-class kinases act within the agrin/MuSK pathway to regulate acetylcholine receptor phosphorylation, cytoskeletal anchoring, and clustering.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2001Article
- Cytoskeletal links of neuronal acetylcholine receptors containing alpha 7 subunits.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2000Article
- Metabolic stabilization of muscle nicotinic acetylcholine receptor by rapsyn.The Journal of neuroscience : the official journal of the Society for Neuroscience · 1999Article
- Axon withdrawal during synapse elimination at the neuromuscular junction is accompanied by disassembly of the postsynaptic specialization and withdrawal of Schwann cell processes.The Journal of neuroscience : the official journal of the Society for Neuroscience · 1998Article
- Subtle neuromuscular defects in utrophin-deficient mice.The Journal of cell biology · 1997Article
- Postsynaptic abnormalities at the neuromuscular junctions of utrophin-deficient mice.The Journal of cell biology · 1997Article
- Increased expression of dystrophin, beta-dystroglycan and adhalin in denervated rat muscles.Journal of muscle research and cell motility · 1996Article
- AChR phosphorylation and aggregation induced by an agrin fragment that lacks the binding domain for alpha-dystroglycan.The EMBO journal · 1996Article
- Molecular and functional analysis of the utrophin promoter.Nucleic acids research · 1996Article
- Distribution of alpha-dystroglycan during embryonic nerve-muscle synaptogenesis.The Journal of cell biology · 1995Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Recombinant acetylcholine receptors (AChRs) expressed on the surface of cultured fibroblasts become organized into discrete membrane domains when the 43-kD postsynaptic protein (43k) is co-expressed in the same cells (Froehner, S.C., C. W. Luetje, P. B. Scotland, and J. Patrick, 1990. Neuron. 5:403-410; Phillips, W. D., M. C. Kopta, P. Blount, P. D. Gardner, J. H. Steinbach, and J. P. Merlie. 1991. Science (Wash. DC). 251:568-570). Here we show that AChRs present on the fibroblast cell surface prior to transfection of 43k are recruited into 43k-rich membrane domains. Aggregated AChRs show increased resistance to extraction with Triton X-100, suggesting a 43k-dependent linkage to the cytoskeleton. Myotubes of the mouse cell line C2 spontaneously display occasional AChR/43k-rich membrane domains that ranged in diameter up to 15 microns, but expressed many more when 43k was overexpressed following transfection of 43k cDNA. However, the membrane domains induced by recombinant 43k were predominantly small (< or = 2 microns). We were then interested in whether the cytoskeletal component, dystrophin related protein (DRP; Tinsley, J. M., D. J. Blake, A. Roche, U. Fairbrother, J. Riss, B. C. Byth, A. E. Knight, J. Kendrick-Jones, G. K. Suthers, D. R. Love, Y. H. Edwards, and K. E. Davis, 1992. Nature (Lond.). 360:591-593) contributed to the development of AChR clusters. Immunofluorescent anti-DRP staining was present at the earliest stages of AChR clustering at the neuromuscular synapse in mouse embryos and was also concentrated at the large AChR-rich domains on nontransfected C2 myotubes. Surprisingly, anti-DRP staining was concentrated mainly at the large, but not the small AChR clusters on C2 myotubes suggesting that DRP may be principally involved in permitting the growth of AChR clusters.
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