ArticleProceedings of the National Academy of Sciences of the United States of America1997
Kinase domain of the muscle-specific receptor tyrosine kinase (MuSK) is sufficient for phosphorylation but not clustering of acetylcholine receptors: required role for the MuSK ectodomain?
Article in Proceedings of the National Academy of Sciences of the United States of America, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 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
32 citing papers in PubMed, 88 citations in OpenAlex.
- IgA autoantibodies demonstrate a novel mechanism of MuSK myasthenia gravis pathology.Brain : a journal of neurology · 2026Article
- A clinical perspective on muscle specific kinase antibody positive myasthenia gravis.Frontiers in immunology · 2024Review
- Review
- MuSK Kinase Activity is Modulated By A Serine Phosphorylation Site in The Kinase Loop.Scientific reports · 2016Article
- Global analysis of muscle-specific kinase signaling by quantitative phosphoproteomics.Molecular & cellular proteomics : MCP · 2014Article
- Altered active zones, vesicle pools, nerve terminal conductivity, and morphology during experimental MuSK myasthenia gravis.PloS one · 2014Article
- Article
- The formation of complex acetylcholine receptor clusters requires MuSK kinase activity and structural information from the MuSK extracellular domain.Molecular and cellular neurosciences · 2012Article
- Molecular control of neuromuscular junction development.Journal of cachexia, sarcopenia and muscle · 2012Article
- Rin-like, a novel regulator of endocytosis, acts as guanine nucleotide exchange factor for Rab5a and Rab22.Biochimica et biophysica acta · 2011Article
- STAT3 activation in skeletal muscle links muscle wasting and the acute phase response in cancer cachexia.PloS one · 2011Article
- LRP4 serves as a coreceptor of agrin.Neuron · 2008Article
- Costameric proteins in human skeletal muscle during muscular inactivity.Journal of anatomy · 2008Article
- Guanylate cyclase and cyclic GMP-dependent protein kinase regulate agrin signaling at the developing neuromuscular junction.Developmental biology · 2007Article
- Analysis of a Shc family adaptor protein, ShcD/Shc4, that associates with muscle-specific kinase.Molecular and cellular biology · 2007Article
- Crystal structure of the agrin-responsive immunoglobulin-like domains 1 and 2 of the receptor tyrosine kinase MuSK.Journal of molecular biology · 2006Article
- Induction of myasthenia by immunization against muscle-specific kinase.The Journal of clinical investigation · 2006Article
- A single pulse of agrin triggers a pathway that acts to cluster acetylcholine receptors.Molecular and cellular biology · 2004Article
- A role for the juxtamembrane domain of beta-dystroglycan in agrin-induced acetylcholine receptor clustering.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2003Article
- MuSK induces in vivo acetylcholine receptor clusters in a ligand-independent manner.The Journal of cell biology · 2001Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Formation of the neuromuscular junction (NMJ) depends upon a nerve-derived protein, agrin, acting by means of a muscle-specific receptor tyrosine kinase, MuSK, as well as a required accessory receptor protein known as MASC. We report that MuSK does not merely play a structural role by demonstrating that MuSK kinase activity is required for inducing acetylcholine receptor (AChR) clustering. We also show that MuSK is necessary, and that MuSK kinase domain activation is sufficient, to mediate a key early event in NMJ formation-phosphorylation of the AChR. However, MuSK kinase domain activation and the resulting AChR phosphorylation are not sufficient for AChR clustering; thus we show that the MuSK ectodomain is also required. These results indicate that AChR phosphorylation is not the sole trigger of the clustering process. Moreover, our results suggest that, unlike the ectodomain of all other receptor tyrosine kinases, the MuSK ectodomain plays a required role in addition to simply mediating ligand binding and receptor dimerization, perhaps by helping to recruit NMJ components to a MuSK-based scaffold.
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.