ArticleFrontiers in cellular neuroscience2014
Frizzled-9 impairs acetylcholine receptor clustering in skeletal muscle cells.
Article in Frontiers in cellular neuroscience, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 14 citations in OpenAlex.
- Crosstalk among canonical Wnt and Hippo pathway members in skeletal muscle and at the neuromuscular junction.Neural regeneration research · 2025Article
- Synergic action of MicroRNAs and Wnts delivered by motor neuron EVs in promoting AChR clustering.Cell communication and signaling : CCS · 2025Article
- 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
- Transport and Secretion of the Wnt3 Ligand by Motor Neuron-like Cells and Developing Motor Neurons.Biomolecules · 2021Article
- Terminal Schwann Cell Aging: Implications for Age-Associated Neuromuscular Dysfunction.Aging and disease · 2021Review
- Deletion of the Williams Beuren syndrome critical region unmasks facioscapulohumeral muscular dystrophy.European journal of paediatric neurology : EJPN : official journal of the European Paediatric Neurology Society · 2020Article
- Frizzled-9+ Supporting Cells Are Progenitors for the Generation of Hair Cells in the Postnatal Mouse Cochlea.Frontiers in molecular neuroscience · 2019Article
- Gene Expression Profiling in Slow-Type Calf Soleus Muscle of 30 Days Space-Flown Mice.PloS one · 2017Article
- Wnt-5a/Frizzled9 Receptor Signaling through the Gαo-Gβγ Complex Regulates Dendritic Spine Formation.The Journal of biological chemistry · 2016Article
- MuSK frizzled-like domain is critical for mammalian neuromuscular junction formation and maintenance.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2015Article
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Authors and funding
10 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cumulative evidence indicates that Wnt pathways play crucial and diverse roles to assemble the neuromuscular junction (NMJ), a peripheral synapse characterized by the clustering of acetylcholine receptors (AChR) on postsynaptic densities. The molecular determinants of Wnt effects at the NMJ are still to be fully elucidated. We report here that the Wnt receptor Frizzled-9 (Fzd9) is expressed in developing skeletal muscles during NMJ synaptogenesis. In cultured myotubes, gain- and loss-of-function experiments revealed that Fzd9-mediated signaling impairs the AChR-clustering activity of agrin, an organizer of postsynaptic differentiation. Overexpression of Fzd9 induced the cytosolic accumulation of β-catenin, a key regulator of Wnt signaling. Consistently, Fzd9 and β-catenin localize in the postsynaptic domain of embryonic NMJs in vivo. Our findings represent the first evidence pointing to a crucial role of a Fzd-mediated, β-catenin-dependent signaling on the assembly of the vertebrate NMJ.
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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.