Evidence map›Paper›PMID 16280586›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2005

Src-family kinases stabilize the neuromuscular synapse in vivo via protein interactions, phosphorylation, and cytoskeletal linkage of acetylcholine receptors.

Gayathri Sadasivam, Raffaella Willmann, Shuo Lin, Susanne Erb-Vögtli, Xian Chu Kong, Markus A Rüegg, Christian Fuhrer

Open access · bronzeAbstract readComparative Study
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
3.0field-weighted citation impact, top 8% of its field
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

34 citing papers in PubMed, 59 citations in OpenAlex.

  1. Review
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  5. The MouseFrontiers in cellular neuroscience · 2020
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  14. Coronin 6 regulates acetylcholine receptor clustering through modulating receptor anchorage to actin cytoskeleton.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2014
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors at 2 institutions in 1 country.

Gayathri SadasivamDepartment of Neurochemistry, Brain Research Institute, University of Zürich, CH-8057 Zürich, Switzerland.
Raffaella Willmann
Shuo Lin
Susanne Erb-Vögtli
Xian Chu Kong
Markus A Rüegg
Christian Fuhrer
University of Zurich · CHUniversity of Basel · CH

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Postnatal stabilization and maturation of the postsynaptic membrane are important for development and function of the neuromuscular junction (NMJ), but the underlying mechanisms remain poorly characterized. We examined the role of Src-family kinases (SFKs) in vivo. Electroporation of kinase-inactive Src constructs into soleus muscles of adult mice caused NMJ disassembly: acetylcholine receptor (AChR)-rich areas became fragmented; the topology of nerve terminal, AChRs, and synaptic nuclei was disturbed; and occasionally nerves started to sprout. Electroporation of kinase-overactive Src produced similar but milder effects. We studied the mechanism of SFK action using cultured src(-/-);fyn(-/-) myotubes, focusing on clustering of postsynaptic proteins, their interaction with AChRs, and AChR phosphorylation. Rapsyn and the utrophin-glycoprotein complex were recruited normally into AChR-containing clusters by agrin in src(-/-);fyn(-/-) myotubes. But after agrin withdrawal, clusters of these proteins disappeared rapidly in parallel with AChRs, revealing that SFKs are of general importance in postsynaptic stability. At the same time, AChR interaction with rapsyn and dystrobrevin and AChR phosphorylation decreased after agrin withdrawal from mutant myotubes. Unexpectedly, levels of rapsyn protein were increased in src(-/-);fyn(-/-) myotubes, whereas rapsyn-cytoskeleton interactions were unaffected. The overall cytoskeletal link of AChRs was weak but still strengthened by agrin in mutant cells, consistent with the normal formation but decreased stability of AChR clusters. These data show that correctly balanced activity of SFKs is critical in maintaining adult NMJs in vivo. SFKs hold the postsynaptic apparatus together through stabilization of AChR-rapsyn interaction and AChR phosphorylation. In addition, SFKs control rapsyn levels and AChR-cytoskeletal linkage.

Indexed as

AgrinAnimalsBungarotoxinsCarrier ProteinsCells, CulturedCytoskeletonDysbindinDystroglycansDystrophin-Associated ProteinsElectroporationGene Expression RegulationGreen Fluorescent ProteinsImaging, Three-DimensionalImmunoblottingImmunohistochemistryIn Vitro TechniquesAgrinBungarotoxinsCarrier ProteinsDtnbp1 protein, mouseDysbindindystrobrevinDystroglycansDystrophin-Associated ProteinsFyn protein, mouseGreen Fluorescent ProteinsMuscle ProteinsNeurofilament Proteinsperipheral membrane protein 43KProto-Oncogene Proteins c-fynReceptors, Cholinergicsrc-Family KinasesSynaptophysinUtrophin

Identifiers

PMID16280586
PMCPMC6725837
OpenAlexW2135158956

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.