ArticleDevelopment (Cambridge, England)2012
β-Catenin gain of function in muscles impairs neuromuscular junction formation.
Article in Development (Cambridge, England), 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 33 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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
33 citing papers in PubMed, 54 citations in OpenAlex.
- Crosstalk among canonical Wnt and Hippo pathway members in skeletal muscle and at the neuromuscular junction.Neural regeneration research · 2025Article
- Spatial transcriptomics in embryonic mouse diaphragm muscle reveals regional gradients and subdomains of developmental gene expression.iScience · 2024Article
- The YAP1/TAZ-TEAD transcriptional network regulates gene expression at neuromuscular junctions in skeletal muscle fibers.Nucleic acids research · 2024Article
- The impact of canonical Wnt transcriptional repressors TLE3 and TLE4 on postsynaptic transcription at the neuromuscular junction.Frontiers in molecular neuroscience · 2024Article
- Mechanical loading is required for initiation of extracellular matrix deposition at the developing murine myotendinous junction.Matrix biology : journal of the International Society for Matrix Biology · 2023Article
- Post-synaptic specialization of the neuromuscular junction: junctional folds formation, function, and disorders.Cell & bioscience · 2022Review
- Article
- Transferrin receptor 1 plays an important role in muscle development and denervation-induced muscular atrophy.Neural regeneration research · 2021Article
- Synapse-specific Lrp4 mRNA enrichment requires Lrp4/MuSK signaling, muscle activity and Wnt non-canonical pathway.Cell & bioscience · 2021Article
- A Role of Lamin A/C in Preventing Neuromuscular Junction Decline in Mice.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2020Article
- Myasthenia Gravis: From the Viewpoint of Pathogenicity Focusing on Acetylcholine Receptor Clustering, Trans-Synaptic Homeostasis and Synaptic Stability.Frontiers in molecular neuroscience · 2020Article
- A mechanism in agrin signaling revealed by a prevalent Rapsyn mutation in congenital myasthenic syndrome.eLife · 2019Article
- Opposite regulation of Wnt/β-catenin and Shh signaling pathways by Rack1 controls mammalian cerebellar development.Proceedings of the National Academy of Sciences of the United States of America · 2019Article
- Rack1 Controls Parallel Fiber-Purkinje Cell Synaptogenesis and Synaptic Transmission.Frontiers in cellular neuroscience · 2019Article
- β-Catenin Controls the Electrophysiologic Properties of Skeletal Muscle Cells by Regulating the α2 Isoform of NaFrontiers in neuroscience · 2019Article
- Differential effects of spinal motor neuron-derived and skeletal muscle-derived Rspo2 on acetylcholine receptor clustering at the neuromuscular junction.Scientific reports · 2018Article
- Article
- Notch1 gain of function in skeletal muscles leads to neuromuscular junction formation defects and neonatal death.CNS neuroscience & therapeutics · 2018Article
- Evolution of the muscular system in tetrapod limbs.Zoological letters · 2018Review
- A novel ALS-associated variant ineLife · 2017Article
Corrections and comments
- Erratum issued
Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
Neuromuscular junction (NMJ) formation requires proper interaction between motoneurons and muscle cells. β-Catenin is required in muscle cells for NMJ formation. To understand underlying mechanisms, we investigated the effect of β-catenin gain of function (GOF) on NMJ development. In HSA-β-cat(flox(ex3)/+) mice, which express stable β-catenin specifically in muscles, motor nerve terminals became extensively defasciculated and arborized. Ectopic muscles were observed in the diaphragm and were innervated by ectopic phrenic nerve branches. Moreover, extensive outgrowth and branching of spinal axons were evident in the GOF mice. These results indicate that increased β-catenin in muscles alters presynaptic differentiation. Postsynaptically, AChR clusters in HSA-β-cat(flox(ex3)/+) diaphragms were distributed in a wider region, suggesting that muscle β-catenin GOF disrupted the signal that restricts AChR clustering to the middle region of muscle fibers. Expression of stable β-catenin in motoneurons, however, had no effect on NMJ formation. These observations provide additional genetic evidence that pre- and postsynaptic development of the NMJ requires an intricate balance of β-catenin activity in muscles.
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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.