ArticleMolecular and cellular biology2004
A single pulse of agrin triggers a pathway that acts to cluster acetylcholine receptors.
Article in Molecular and cellular biology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 50 citations in OpenAlex.
- Five key challenges for the plasma membrane insertion of nicotinic acetylcholine receptors in cellular model systems.Molecular and cellular biochemistry · 2026Review
- Modulation of a rapid neurotransmitter receptor-ion channel by membrane lipids.Frontiers in cell and developmental biology · 2023Review
- Creating stem cell-derived neuromuscular junctions in vitro.Muscle & nerve · 2021Review
- 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
- Global analysis of muscle-specific kinase signaling by quantitative phosphoproteomics.Molecular & cellular proteomics : MCP · 2014Article
- Muscle-specific kinase (MuSK) autoantibodies suppress the MuSK pathway and ACh receptor retention at the mouse neuromuscular junction.The Journal of physiology · 2014Article
- Molecular control of neuromuscular junction development.Journal of cachexia, sarcopenia and muscle · 2012Article
- Current status of the congenital myasthenic syndromes.Neuromuscular disorders : NMD · 2012Review
- Role of extracellular matrix proteins and their receptors in the development of the vertebrate neuromuscular junction.Developmental neurobiology · 2011Review
- Article
- Modulation of agrin-induced acetylcholine receptor clustering by extracellular signal-regulated kinases 1 and 2 in cultured myotubes.The Journal of biological chemistry · 2010Article
- alpha-Actinin interacts with rapsyn in agrin-stimulated AChR clustering.Molecular brain · 2008Article
- Article
- The function of Shp2 tyrosine phosphatase in the dispersal of acetylcholine receptor clusters.BMC neuroscience · 2008Article
- Rapsyn carboxyl terminal domains mediate muscle specific kinase-induced phosphorylation of the muscle acetylcholine receptor.Neuroscience · 2008Article
- Tyrosine phosphatases such as SHP-2 act in a balance with Src-family kinases in stabilization of postsynaptic clusters of acetylcholine receptors.BMC neuroscience · 2007Article
- Analysis of a Shc family adaptor protein, ShcD/Shc4, that associates with muscle-specific kinase.Molecular and cellular biology · 2007Article
- Regulation of synaptic growth and maturation by a synapse-associated E3 ubiquitin ligase at the neuromuscular junction.The Journal of cell biology · 2007Article
- Cholesterol and lipid microdomains stabilize the postsynapse at the neuromuscular junction.The EMBO journal · 2006Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
Abstract
Agrin triggers signaling mechanisms of high temporal and spatial specificity to achieve phosphorylation, clustering, and stabilization of postsynaptic acetylcholine receptors (AChRs). Agrin transiently activates the kinase MuSK; MuSK activation has largely vanished when AChR clusters appear. Thus, a tyrosine kinase cascade acts downstream from MuSK, as illustrated by the agrin-evoked long-lasting activation of Src family kinases (SFKs) and their requirement for AChR cluster stabilization. We have investigated this cascade and report that pharmacological inhibition of SFKs reduces early but not later agrin-induced phosphorylation of MuSK and AChRs, while inhibition of Abl kinases reduces late phosphorylation. Interestingly, SFK inhibition applied selectively during agrin-induced AChR cluster formation caused rapid cluster dispersal later upon agrin withdrawal. We also report that a single 5-min agrin pulse, followed by extensive washing, triggered long-lasting MuSK and AChR phosphorylation and efficient AChR clustering. Following the pulse, MuSK phosphorylation increased and, beyond a certain level, caused maximal clustering. These data reveal novel temporal aspects of tyrosine kinase action in agrin signaling. First, during AChR cluster formation, SFKs initiate early phosphorylation and an AChR stabilization program that acts much later. Second, a kinase mechanism rapidly activated by agrin acts thereafter autonomously in agrin's absence to further increase MuSK phosphorylation and cluster AChRs.
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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.