Evidence map›Paper›PMID 10995438›Full record

ArticleThe Journal of cell biology2000

The actin-driven movement and formation of acetylcholine receptor clusters.

Z Dai, X Luo, H Xie, H B Peng

Abstract read
In one paragraph

Article in The Journal of cell biology, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 71 papers.

0numbers the graph read from it
0cells of the map it votes in
71citing papers in PubMed
–field-weighted citation impact
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

71 citing papers in PubMed.

  1. Article
  2. Review
  3. Review
  4. Article
  5. Review
  6. Article
  7. Aberrant evoked calcium signaling and nAChR cluster morphology in aFrontiers in cell and developmental biology · 2024
    Article
  8. Review
  9. Article
  10. Article
  11. Article
  12. Review
  13. Article
  14. Article
  15. Article
  16. Review
  17. Article
  18. Muscle-Specific Kinase Myasthenia Gravis.Frontiers in immunology · 2020
    Review
  19. Article
  20. Review

11 more citing papers are in PubMed but not listed here.

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

4 authors.

Z DaiDepartment of Cell Biology and Anatomy, University of North Carolina, Chapel Hill, North Carolina 27599, USA.
X Luo
H Xie
H B Peng

Funding

DEVELOPMENT OF THE SYNAPSER01NS023583 · NINDS · UNIVERSITY OF NORTH CAROLINA CHAPEL HILL · PI PENG, HSIAO-MING B · 1985 to 2002
$710k
NINDS NIH HHS NS23583NINDS NIH HHS R01 NS023583
6 · The paper itself

Abstract

A new method was devised to visualize actin polymerization induced by postsynaptic differentiation signals in cultured muscle cells. This entails masking myofibrillar filamentous (F)-actin with jasplakinolide, a cell-permeant F-actin-binding toxin, before synaptogenic stimulation, and then probing new actin assembly with fluorescent phalloidin. With this procedure, actin polymerization associated with newly induced acetylcholine receptor (AChR) clustering by heparin-binding growth-associated molecule-coated beads and by agrin was observed. The beads induced local F-actin assembly that colocalized with AChR clusters at bead-muscle contacts, whereas both the actin cytoskeleton and AChR clusters induced by bath agrin application were diffuse. By expressing a green fluorescent protein-coupled version of cortactin, a protein that binds to active F-actin, the dynamic nature of the actin cytoskeleton associated with new AChR clusters was revealed. In fact, the motive force generated by actin polymerization propelled the entire bead-induced AChR cluster with its attached bead to move in the plane of the membrane. In addition, actin polymerization is also necessary for the formation of both bead and agrin-induced AChR clusters as well as phosphotyrosine accumulation, as shown by their blockage by latrunculin A, a toxin that sequesters globular (G)-actin and prevents F-actin assembly. These results show that actin polymerization induced by synaptogenic signals is necessary for the movement and formation of AChR clusters and implicate a role of F-actin as a postsynaptic scaffold for the assembly of structural and signaling molecules in neuromuscular junction formation.

Indexed as

DepsipeptidesActinsAnimalsAntineoplastic AgentsBridged Bicyclo Compounds, HeterocyclicCells, CulturedCortactinGene ExpressionGenes, ReporterGreen Fluorescent ProteinsIndicators and ReagentsLuminescent ProteinsMicrofilament ProteinsMicrospheresMusclesNeuromuscular JunctionActinsAntineoplastic AgentsBridged Bicyclo Compounds, HeterocyclicCortactinDepsipeptidesGreen Fluorescent ProteinsIndicators and Reagentsjasplakinolidelatrunculin ALuminescent ProteinsMicrofilament ProteinsPeptides, CyclicPolymersReceptors, CholinergicThiazolesThiazolidines

Identifiers

PMID10995438
PMCPMC2150690

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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.