ArticleThe Journal of cell biology2002
Laminin-1 redistributes postsynaptic proteins and requires rapsyn, tyrosine phosphorylation, and Src and Fyn to stably cluster acetylcholine receptors.
Article in The Journal of cell biology, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
15 citing papers in PubMed, 48 citations in OpenAlex.
- Fyn Signaling in Ischemia-Reperfusion Injury: Potential and Therapeutic Implications.Mediators of inflammation · 2022Review
- The Laminin-Induced Phosphorylation of PKCδ Regulates AQP4 Distribution and Water Permeability in Rat Astrocytes.Cellular and molecular neurobiology · 2021Article
- Scale Invariant Disordered Nanotopography Promotes Hippocampal Neuron Development and Maturation with Involvement of Mechanotransductive Pathways.Frontiers in cellular neuroscience · 2016Article
- Integrated genomics and proteomics of the Torpedo californica electric organ: concordance with the mammalian neuromuscular junction.Skeletal muscle · 2011Article
- Interdependence of laminin-mediated clustering of lipid rafts and the dystrophin complex in astrocytes.The Journal of biological chemistry · 2009Article
- Presynaptic secretion of mind-the-gap organizes the synaptic extracellular matrix-integrin interface and postsynaptic environments.Developmental dynamics : an official publication of the American Association of Anatomists · 2009Article
- Laminins promote postsynaptic maturation by an autocrine mechanism at the neuromuscular junction.The Journal of cell biology · 2008Article
- Tyrosine phosphatases such as SHP-2 act in a balance with Src-family kinases in stabilization of postsynaptic clusters of acetylcholine receptors.BMC neuroscience · 2007Article
- Cholesterol and lipid microdomains stabilize the postsynapse at the neuromuscular junction.The EMBO journal · 2006Article
- Induction of myasthenia by immunization against muscle-specific kinase.The Journal of clinical investigation · 2006Article
- Regulation of dendritic branching and spine maturation by semaphorin3A-Fyn signaling.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2006Article
- Src-family kinases stabilize the neuromuscular synapse in vivo via protein interactions, phosphorylation, and cytoskeletal linkage of acetylcholine receptors.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2005Article
- Beta1 integrins in muscle, but not in motor neurons, are required for skeletal muscle innervation.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2004Article
- A single pulse of agrin triggers a pathway that acts to cluster acetylcholine receptors.Molecular and cellular biology · 2004Article
- Nerve-independent formation of a topologically complex postsynaptic apparatus.The Journal of cell biology · 2004Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Clustering of acetylcholine receptors (AChRs) is a critical step in neuromuscular synaptogenesis, and is induced by agrin and laminin which are thought to act through different signaling mechanisms. We addressed whether laminin redistributes postsynaptic proteins and requires key elements of the agrin signaling pathway to cause AChR aggregation. In myotubes, laminin-1 rearranged dystroglycans and syntrophins into a laminin-like network, whereas inducing AChR-containing clusters of dystrobrevin, utrophin, and, to a marginal degree, MuSK. Laminin-1 also caused extensive coclustering of rapsyn and phosphotyrosine with AChRs, but none of these clusters were observed in rapsyn -/- myotubes. In parallel with clustering, laminin-1 induced tyrosine phosphorylation of AChR beta and delta subunits. Staurosporine and herbimycin, inhibitors of tyrosine kinases, prevented laminin-induced AChR phosphorylation and AChR and phosphotyrosine clustering, and caused rapid dispersal of clusters previously induced by laminin-1. Finally, laminin-1 caused normal aggregation of AChRs and phosphotyrosine in myotubes lacking both Src and Fyn kinases, but these clusters dispersed rapidly after laminin withdrawal. Thus, laminin-1 redistributes postsynaptic proteins and, like agrin, requires tyrosine kinases for AChR phosphorylation and clustering, and rapsyn for AChR cluster formation, whereas cluster stabilization depends on Src and Fyn. Therefore, the laminin and agrin signaling pathways overlap intracellularly, which may be important for neuromuscular synapse formation.
Indexed as
Identifiers
What OpenQuestion holds
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.