Evidence map›Paper›PMID 9254666›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience1997

Neural agrin induces ectopic postsynaptic specializations in innervated muscle fibers.

T Meier, D M Hauser, M Chiquet, L Landmann, M A Ruegg, H R Brenner

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed
4.4field-weighted citation impact, top 4% 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

38 citing papers in PubMed, 131 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. A Role of Lamin A/C in Preventing Neuromuscular Junction Decline in Mice.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2020
    Article
  6. Review
  7. Review
  8. Article
  9. Article
  10. LRP4 is critical for neuromuscular junction maintenance.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2014
    Article
  11. Article
  12. Basement membranes: cell scaffoldings and signaling platforms.Cold Spring Harbor perspectives in biology · 2011
    Review
  13. Article
  14. Article
  15. 14-3-3 gamma associates with muscle specific kinase and regulates synaptic gene transcription at vertebrate neuromuscular synapse.Proceedings of the National Academy of Sciences of the United States of America · 2004
    Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Review
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

6 authors at 2 institutions in 1 country.

T MeierInstitute of Physiology, University of Basel, CH-4051 Basel, Switzerland.
D M Hauser
M Chiquet
L Landmann
M A Ruegg
H R Brenner
University of Basel · CHUniversity of Bern · CH

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Neural agrin, in the absence of a nerve terminal, can induce the activity-resistant expression of acetylcholine receptor (AChR) subunit genes and the clustering of synapse-specific adult-type AChR channels in nonsynaptic regions of adult skeletal muscle fibers. Here we show that, when expression plasmids for neural agrin are injected into the extrasynaptic region of innervated muscle fibers, the following components of the postsynaptic apparatus are aggregated and colocalized with ectopic agrin-induced AChR clusters: laminin-beta2, MuSK, phosphotyrosine-containing proteins, beta-dystroglycan, utrophin, and rapsyn. These components have been implicated to play a role in the differentiation of neuromuscular junctions. Furthermore, ErbB2 and ErbB3, which are thought to be involved in the regulation of neurally induced AChR subunit gene expression, were colocalized with agrin-induced AChR aggregates at ectopic nerve-free sites. The postsynaptic muscle membrane also contained a high concentration of voltage-gated Na+ channels as well as deep, basal lamina-containing invaginations comparable to the secondary synaptic folds of normal endplates. The ability to induce AChR aggregation in vivo was not observed in experiments with a muscle-specific agrin isoform. Thus, a motor neuron-specific agrin isoform is sufficient to induce a full ectopic postsynaptic apparatus in muscle fibers kept electrically active at their original endplate sites.

Indexed as

AgrinAnimalsChickensElectrophysiologyErb-b2 Receptor Tyrosine KinasesErbB ReceptorsMotor EndplateMuscle Fibers, SkeletalMusclesNerve TissueNerve Tissue ProteinsRatsReceptor AggregationReceptor Protein-Tyrosine KinasesReceptors, CholinergicSodium ChannelsAgrinErb-b2 Receptor Tyrosine KinasesErbB ReceptorsNerve Tissue ProteinsReceptor Protein-Tyrosine KinasesReceptors, CholinergicSodium Channels

Identifiers

PMID9254666
PMCPMC6573144
OpenAlexW1852588865

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.