ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2010
The alpha-syntrophin PH and PDZ domains scaffold acetylcholine receptors, utrophin, and neuronal nitric oxide synthase at the neuromuscular junction.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 39 citations in OpenAlex.
- The role of dystrophin isoforms and interactors in the brain.Brain : a journal of neurology · 2025Review
- Temporal Regulation of Myopia and Inflammation-Associated Pathways in the Interphotoreceptor Retinoid-Binding Protein Knockout Mouse Model.Current eye research · 2025Article
- Inhibition of p38α MAPK restores neuronal p38γ MAPK and ameliorates synaptic degeneration in a mouse model of DLB/PD.Science translational medicine · 2023Article
- 2023 Padua Days of Muscle and Mobility Medicine: post-meeting Book of Abstracts.European journal of translational myology · 2023Article
- Abstracts of the 2023 Padua Days of Muscle and Mobility Medicine (2023Pdm3) to be held March 29 - April 1 at the Galileian Academy of Padua and at the Petrarca Hotel, Thermae of Euganean Hills, Padua, Italy.European journal of translational myology · 2023Article
- A link between agrin signalling and CaScientific reports · 2022Article
- Distinct roles of the dystrophin-glycoprotein complex: α-dystrobrevin and α-syntrophin in the maintenance of the postsynaptic apparatus of the neuromuscular synapse.Human molecular genetics · 2022Article
- Learning peptide recognition rules for a low-specificity protein.Protein science : a publication of the Protein Society · 2020Article
- Recent insights into neuromuscular junction biology in Duchenne muscular dystrophy: Impacts, challenges, and opportunities.EBioMedicine · 2020Review
- Microutrophin expression in dystrophic mice displays myofiber type differences in therapeutic effects.PLoS genetics · 2020Article
- The role of the dystrophin glycoprotein complex on the neuromuscular system.Neuroscience letters · 2020Review
- Syntrophin binds directly to multiple spectrin-like repeats in dystrophin and mediates binding of nNOS to repeats 16-17.Human molecular genetics · 2018Article
- Skeletal muscle in aged mice reveals extensive transformation of muscle gene expression.BMC genetics · 2018Article
- Biochemical and Functional Interplay Between Ion Channels and the Components of the Dystrophin-Associated Glycoprotein Complex.The Journal of membrane biology · 2018Review
- A Genome-Wide Association Study IdentifiesPsychiatry investigation · 2017Article
- MicroRNAs promote skeletal muscle differentiation of mesodermal iPSC-derived progenitors.Nature communications · 2017Article
- Spatial distribution and molecular dynamics of dystrophin glycoprotein components at the neuromuscular junctionJournal of cell science · 2017Article
- A Hypothesis for Examining Skeletal Muscle Biopsy-Derived Sarcolemmal nNOSμ as Surrogate for Enteric nNOSα Function.Frontiers in medicine · 2015Article
- Dystroglycan mediates homeostatic synaptic plasticity at GABAergic synapses.Proceedings of the National Academy of Sciences of the United States of America · 2014Article
- Protein kinase D interacts with neuronal nitric oxide synthase and phosphorylates the activatory residue serine 1412.PloS one · 2014Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
At the neuromuscular junction (NMJ), the dystrophin protein complex provides a scaffold that functions to stabilize acetylcholine receptor (AChR) clusters. Syntrophin, a key component of that scaffold, is a multidomain adapter protein that links a variety of signaling proteins and ion channels to the dystrophin protein complex. Without syntrophin, utrophin and neuronal nitric oxide synthase mu (nNOSmu) fail to localize to the NMJ and the AChRs are distributed abnormally. Here we investigate the contribution of syntrophin domains to AChR distribution and to localization of utrophin and nNOSmu at the NMJ. Transgenic mice expressing alpha-syntrophin lacking portions of the first pleckstrin homology (PH) domain (DeltaPH1a or DeltaPH1b) or the entire PDZ domain (DeltaPDZ) were bred onto the alpha-syntrophin null background. As expected the DeltaPDZ transgene did not restore the NMJ localization of nNOS. The DeltaPH1a transgene did restore postsynaptic nNOS but surprisingly did not restore sarcolemmal nNOS (although sarcolemmal aquaporin-4 was restored). Mice lacking the alpha-syntrophin PDZ domain or either half of the PH1 domain were able to restore utrophin to the NMJ but did not correct the aberrant AChR distribution of the alpha-syntrophin knock-out mice. However, mice expressing both the transgenic DeltaPDZ and the transgenic DeltaPH1a constructs did restore normal AChR distribution, demonstrating that both domains are required but need not be confined within the same protein to function. We conclude that the PH1 and PDZ domains of alpha-syntrophin work in concert to facilitate the localization of AChRs and nNOS at the 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.