ArticleThe Journal of cell biology2000
Agrin-induced acetylcholine receptor clustering is mediated by the small guanosine triphosphatases Rac and Cdc42.
Article in The Journal of cell biology, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 62 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
62 citing papers in PubMed, 146 citations in OpenAlex.
- Five key challenges for the plasma membrane insertion of nicotinic acetylcholine receptors in cellular model systems.Molecular and cellular biochemistry · 2026Review
- Protein networking: nicotinic acetylcholine receptors and their protein-protein-associations.Molecular and cellular biochemistry · 2024Review
- Building, Breaking, and Repairing Neuromuscular Synapses.Cold Spring Harbor perspectives in biology · 2024Review
- Maturation of a postsynaptic domain: Role of small Rho GTPases in organising nicotinic acetylcholine receptor aggregates at the vertebrate neuromuscular junction.Journal of anatomy · 2022Review
- Control of CRK-RAC1 activity by the miR-1/206/133 miRNA family is essential for neuromuscular junction function.Nature communications · 2022Article
- Drebrin Regulates Acetylcholine Receptor Clustering and Organization of Microtubules at the Postsynaptic Machinery.International journal of molecular sciences · 2021Article
- An Inside Job: Molecular Determinants for Postsynaptic Localization of Nicotinic Acetylcholine Receptors.Molecules (Basel, Switzerland) · 2021Review
- Possible implications of dysregulated nicotinic acetylcholine receptor diffusion and nanocluster formation in myasthenia gravis.Neural regeneration research · 2021Review
- Regulatory Function of Sympathetic Innervation on the Endo/Lysosomal Trafficking of Acetylcholine Receptor.Frontiers in physiology · 2021Article
- Review
- A Role for Caveolin-3 in the Pathogenesis of Muscular Dystrophies.International journal of molecular sciences · 2020Review
- Arhgef5 Binds α-Dystrobrevin 1 and Regulates Neuromuscular Junction Integrity.Frontiers in molecular neuroscience · 2020Article
- Fundamental Molecules and Mechanisms for Forming and Maintaining Neuromuscular Synapses.International journal of molecular sciences · 2018Review
- Muscle Yap Is a Regulator of Neuromuscular Junction Formation and Regeneration.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2017Article
- Protein kinase CK2 interacts at the neuromuscular synapse with Rapsyn, Rac1, 14-3-3γ, and Dok-7 proteins and phosphorylates the latter two.The Journal of biological chemistry · 2015Article
- Impaired Synaptic Development, Maintenance, and Neuromuscular Transmission in LRP4-Related Myasthenia.JAMA neurology · 2015Article
- Postsynaptic assembly: a role for Wnt signaling.Developmental neurobiology · 2014Review
- The role of MuSK in synapse formation and neuromuscular disease.Cold Spring Harbor perspectives in biology · 2013Review
- Nestin negatively regulates postsynaptic differentiation of the neuromuscular synapse.Nature neuroscience · 2011Article
- Emerging roles for MAP kinases in agrin signaling.Communicative & integrative biology · 2011Article
2 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
During neuromuscular junction formation, agrin secreted from motor neurons causes muscle cell surface acetylcholine receptors (AChRs) to cluster at synaptic sites by mechanisms that are insufficiently understood. The Rho family of small guanosine triphosphatases (GTPases), including Rac and Cdc42, can mediate focal reorganization of the cell periphery in response to extracellular signals. Here, we investigated the role of Rac and Cdc42 in coupling agrin signaling to AChR clustering. We found that agrin causes marked muscle-specific activation of Rac and Cdc42 in differentiated myotubes, as detected by biochemical measurements. Moreover, this activation is crucial for AChR clustering, since the expression of dominant interfering mutants of either Rac or Cdc42 in myotubes blocks agrin-induced AChR clustering. In contrast, constitutively active Rac and Cdc42 mutants cause AChR to aggregate in the absence of agrin. By indicating that agrin-dependent activation of Rac and Cdc42 constitutes a critical step in the signaling pathway leading to AChR clustering, these findings suggest a novel role for these Rho-GTPases: the coupling of neuronal signaling to a key step in neuromuscular synaptogenesis.
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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.