ArticleProceedings of the National Academy of Sciences of the United States of America2008
Muscle-wide secretion of a miniaturized form of neural agrin rescues focal neuromuscular innervation in agrin mutant mice.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2008. 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, 45 citations in OpenAlex.
- Laminins and the blood-brain barrier.Matrix biology : journal of the International Society for Matrix Biology · 2025Review
- Severe congenital myasthenic syndromes caused by agrin mutations affecting secretion by motoneurons.Acta neuropathologica · 2022Article
- Muscle-Specific Cellular and Molecular Adaptations to Late-Life Voluntary Concurrent Exercise.Function (Oxford, England) · 2022Article
- Light Cross-Linkable Marine Collagen for Coaxial Printing of a 3D Model of Neuromuscular Junction Formation.Biomedicines · 2020Article
- Basement Membrane Changes in Ischemic Stroke.Stroke · 2020Review
- Spatiotemporal Distribution of Agrin after Intrathecal Injection and Its Protective Role in Cerebral Ischemia/Reperfusion Injury.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2020Article
- Modulation of the Acetylcholine Receptor Clustering Pathway Improves Neuromuscular Junction Structure and Muscle Strength in a Mouse Model of Congenital Myasthenic Syndrome.Frontiers in molecular neuroscience · 2020Article
- A Novel Egr-1-Agrin Pathway and Potential Implications for Regulation of Synaptic Physiology and Homeostasis at the Neuromuscular Junction.Frontiers in aging neuroscience · 2017Article
- Decoding the Matrix: Instructive Roles of Proteoglycan Receptors.Biochemistry · 2015Review
- The MuSK activator agrin has a separate role essential for postnatal maintenance of neuromuscular synapses.Proceedings of the National Academy of Sciences of the United States of America · 2014Article
- The heparan sulfate proteoglycan agrin contributes to barrier properties of mouse brain endothelial cells by stabilizing adherens junctions.Cell and tissue research · 2014Article
- LRP4 is critical for neuromuscular junction maintenance.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2014Article
- Bone morphogenetic protein signaling in vertebrate motor neurons and neuromuscular communication.Frontiers in cellular neuroscience · 2014Review
- Article
- Soluble miniagrin enhances contractile function of engineered skeletal muscle.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2012Article
- Nestin negatively regulates postsynaptic differentiation of the neuromuscular synapse.Nature neuroscience · 2011Article
- Basement membranes: cell scaffoldings and signaling platforms.Cold Spring Harbor perspectives in biology · 2011Review
- Extracellular matrix: functions in the nervous system.Cold Spring Harbor perspectives in biology · 2011Review
- Identification of an agrin mutation that causes congenital myasthenia and affects synapse function.American journal of human genetics · 2009Article
- Basement membrane proteoglycans: modulators Par Excellence of cancer growth and angiogenesis.Molecules and cells · 2009Review
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Agrin and its receptor MuSK are required for the formation of the postsynaptic apparatus at the neuromuscular junction (NMJ). In the current model the local deposition of agrin by the nerve and the resulting local activation of MuSK are responsible for creating and maintaining the postsynaptic apparatus including clusters of acetylcholine receptors (AChRs). Concomitantly, the release of acetylcholine (ACh) and the resulting depolarization disperses those postsynaptic structures that are not apposed by the nerve and thus not stabilized by agrin-MuSK signaling. Here we show that a miniaturized form of agrin, consisting of the laminin-binding and MuSK-activating domains, is sufficient to fully restore NMJs in agrin mutant mice when expressed by developing muscle. Although miniagrin is expressed uniformly throughout muscle fibers and induces ectopic AChR clusters, the size and the number of those AChR clusters contacted by the motor nerve increase during development. We provide experimental evidence that this is due to ACh, because the AChR agonist carbachol stabilizes AChR clusters in organotypic cultures of embryonic diaphragms. In summary, our results show that agrin function in NMJ development requires only two small domains, and that this function does not depend on the local deposition of agrin at synapses. Finally, they suggest a novel local function of ACh in stabilizing postsynaptic structures.
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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.