Evidence map›Paper›PMID 9454855›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience1998

Organization and reorganization of neuromuscular junctions in mice lacking neural cell adhesion molecule, tenascin-C, or fibroblast growth factor-5.

L M Moscoso, H Cremer, J R Sanes

Abstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing 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

28 citing papers in PubMed.

  1. Article
  2. FGF5 Regulates Schwann Cell Migration and Adhesion.Frontiers in cellular neuroscience · 2020
    Article
  3. Review
  4. Article
  5. Perspectives in Diagnosis and Treatment of Rabies Viral Encephalitis: Insights from Pathogenesis.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2016
    Review
  6. Article
  7. Polyclonal neural cell adhesion molecule antibody prolongs the effective duration time of botulinum toxin in decreasing muscle strength.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2015
    Article
  8. Article
  9. Article
  10. Article
  11. Review
  12. Article
  13. Article
  14. Presynaptic and postsynaptic interaction of the amyloid precursor protein promotes peripheral and central synaptogenesis.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2009
    Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Polysialylated neural cell adhesion molecule is necessary for selective targeting of regenerating motor neurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2005
    Article
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

3 authors.

L M MoscosoDepartment of Anatomy and Neurobiology, Washington University School of Medicine, St. Louis, Missouri 63110, USA.
H Cremer
J R Sanes

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Many proteins have been hypothesized to mediate intercellular interactions that regulate the formation, maturation, and maintenance of the skeletal neuromuscular junction. Three of the best characterized of these are a membrane-associated adhesion molecule, neural cell adhesion molecule (N-CAM), an extracellular matrix component, tenascin-C, and a soluble growth factor, fibroblast growth factor-5 (FGF-5). To assess the roles of these molecules in synaptogenesis in vivo, we examined neuromuscular junctions in homozygous mutant mice lacking N-CAM, tenascin-C, FGF-5, or both N-CAM and tenascin-C. End plates were 14% smaller in N-CAM-deficient mice than in controls, and formation of junctional folds was delayed in this mutant. In all other respects tested, however, the structure and molecular architecture of neuromuscular junctions were normal in all three single mutants and in the double mutant. We also tested the abilities of damaged motor axons to reinnervate mutant muscle after axotomy and of intact motor axons to sprout after partial denervation. Again, no significant differences among genotypes were observed. Together, these results demonstrate that N-CAM, tenascin-C, and FGF-5 are dispensable for major aspects of synaptic development and regeneration.

Indexed as

AnimalsFibroblast Growth Factor 5Fibroblast Growth FactorsMiceMice, Inbred C57BLMice, Neurologic MutantsMutationNeural Cell Adhesion MoleculesNeuromuscular JunctionNeuronal PlasticityTenascinFgf5 protein, mouseFibroblast Growth Factor 5Fibroblast Growth FactorsNeural Cell Adhesion MoleculesTenascin

Identifiers

PMID9454855
PMCPMC6792746

What OpenQuestion holds

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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.