Evidence map›Paper›PMID 16407563›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2006

Neuromuscular synapse formation in mice lacking motor neuron- and skeletal muscle-derived Neuregulin-1.

Alexander Jaworski, Steven J Burden

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed
3.5field-weighted citation impact, top 7% 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

42 citing papers in PubMed, 92 citations in OpenAlex.

  1. Article
  2. Building, Breaking, and Repairing Neuromuscular Synapses.Cold Spring Harbor perspectives in biology · 2024
    Review
  3. Article
  4. Article
  5. Review
  6. Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Review
  12. Article
  13. Neuregulin1 fine-tunes pre-, post-, and perisynaptic neuromuscular junction development.Developmental dynamics : an official publication of the American Association of Anatomists · 2017
    Article
  14. Article
  15. Schwann Cells in Neuromuscular Junction Formation and Maintenance.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2016
    Article
  16. Article
  17. Article
  18. Review
  19. Article
  20. 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

2 authors at 1 institution in 1 country.

Alexander JaworskiMolecular Neurobiology Program, Skirball Institute of Biomolecular Medicine, New York University School of Medicine, New York, New York 10016, USA.
Steven J Burden
New York University · US

Funding

REGULATION OF ACHR GENE EXPRESSION--ELECTRICAL ACTIVITYR01NS027963 · NINDS · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI BURDEN, STEVEN · 1990 to 2004
$2.1M
NINDS NIH HHS R01 NS027963
6 · The paper itself

Abstract

The localization of acetylcholine receptors (AChRs) to the vertebrate neuromuscular junction is mediated, in part, through selective transcription of AChR subunit genes in myofiber subsynaptic nuclei. Agrin and the muscle-specific receptor tyrosine kinase, MuSK, have critical roles in synapse-specific transcription, because AChR genes are expressed uniformly in mice lacking either agrin or MuSK. Several lines of evidence suggest that agrin and MuSK stimulate synapse-specific transcription indirectly by regulating the distribution of other cell surface ligands, which stimulate a pathway for synapse-specific gene expression. This putative secondary signal for directing AChR gene expression to synapses is not known, but Neuregulin-1 (Nrg-1), primarily based on its presence at synapses and its ability to induce AChR gene expression in vitro, has been considered a good candidate. To study the role of Nrg-1 at neuromuscular synapses, we inactivated nrg-1 in motor neurons, skeletal muscle, or both cell types, using mice that express Cre recombinase selectively in developing motor neurons or in developing skeletal myofibers. We find that AChRs are clustered at synapses and that synapse-specific transcription is normal in mice lacking Nrg-1 in motor neurons, myofibers, or both cell types. These data indicate that Nrg-1 is dispensable for clustering AChRs and activating AChR genes in subsynaptic nuclei during development and suggest that these aspects of postsynaptic differentiation are dependent on Agrin/MuSK signaling without a requirement for a secondary signal.

Indexed as

AgrinAnimalsbeta-GalactosidaseCell DifferentiationDiaphragmErb-b2 Receptor Tyrosine KinasesErbB ReceptorsGenes, ReporterIntegrasesIntercostal MusclesMiceMice, KnockoutMotor NeuronsMuscle Fibers, SkeletalMuscle, SkeletalNerve Tissue ProteinsAgrinbeta-GalactosidaseCre recombinaseErb-b2 Receptor Tyrosine KinasesERBB4 protein, humanErbb4 protein, mouseErbB ReceptorsIntegrasesMUSK protein, humanNerve Tissue ProteinsNeuregulin-1Nrg1 protein, mouseReceptor, ErbB-4Receptor Protein-Tyrosine KinasesReceptors, CholinergicRNA, MessengerViral Proteins

Identifiers

PMID16407563
PMCPMC6674415
OpenAlexW2009355776

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.