ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2003
A role for the juxtamembrane domain of beta-dystroglycan in agrin-induced acetylcholine receptor clustering.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 22 citations in OpenAlex.
- Extracellular signal-regulated kinases 1 and 2 regulate neuromuscular junction and myofiber phenotypes in mammalian skeletal muscle.Neuroscience letters · 2020Review
- Muscle-specific kinase (MuSK) autoantibodies suppress the MuSK pathway and ACh receptor retention at the mouse neuromuscular junction.The Journal of physiology · 2014Article
- Modulation of agrin-induced acetylcholine receptor clustering by extracellular signal-regulated kinases 1 and 2 in cultured myotubes.The Journal of biological chemistry · 2010Article
- Dystroglycan versatility in cell adhesion: a tale of multiple motifs.Cell communication and signaling : CCS · 2010Article
- The conserved WW-domain binding sites in Dystroglycan C-terminus are essential but partially redundant for Dystroglycan function.BMC developmental biology · 2009Article
- Nuclear translocation of beta-dystroglycan reveals a distinctive trafficking pattern of autoproteolyzed mucins.Traffic (Copenhagen, Denmark) · 2008Article
- Dp71, utrophin and beta-dystroglycan expression and distribution in PC12/L6 cell cocultures.Neuroreport · 2007Article
- 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
- Complete deletion of all alpha-dystrobrevin isoforms does not reveal new neuromuscular junction phenotype.Gene expression · 2007Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Synaptic differentiation results from an exchange of informational molecules between synaptic partners during development. At the vertebrate neuromuscular junction, agrin is one molecule presented by the presynaptic motor neuron that plays an instructive role in postsynaptic differentiation of the muscle cell, most notably in aggregation of acetylcholine receptors (AChRs). Although agrin is the best-characterized synaptogenic molecule, its mechanism of action remains uncertain, but clearly, it requires the receptor tyrosine kinase MuSK (muscle-specific kinase), the intracellular protein rapsyn, an Src-like kinase, and cytoskeletal components. In addition, the transmembrane protein dystroglycan interacts with the cytoskeleton and is implicated in agrin responsiveness. This alpha-beta heterodimer can bind agrin via its extracellular alpha subunit and associates with the membrane cytoskeleton via its beta subunit. In this study, we demonstrate that overexpression of the beta subunit of dystroglycan in cultured muscle cells inhibits agrin-induced AChR clustering. Deletion analysis and point mutagenesis demonstrate that the inhibition is mediated by an intracellular, juxtamembrane region composed of basic amino acids. Finally, the inhibition mediated by beta-dystroglycan extends to the minimal agrin fragment required for AChR clustering, suggesting that dystroglycan plays an important role in postsynaptic differentiation in response to agrin.
Indexed as
Identifiers
12533599PMC6741885W1517693690What 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.