Evidence map›Paper›PMID 23637281›Full record

ReviewCold Spring Harbor perspectives in biology2013

The role of MuSK in synapse formation and neuromuscular disease.

Steven J Burden, Norihiro Yumoto, Wei Zhang

Open access · bronzeAbstract readReview
In one paragraph

Review in Cold Spring Harbor perspectives in biology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 94 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
94citing papers in PubMed, 1 pooled it
–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

94 citing papers in PubMed, 1 synthesis or guideline pooled it, 183 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. MuSK IgG4 autoantibodies cause myasthenia gravis by inhibiting binding between MuSK and Lrp4.Proceedings of the National Academy of Sciences of the United States of America · 2013
    Trial
  4. NMJ-associated transcriptomic remodeling correlates with disease severity in juvenile dermatomyositis.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026
    Article
  5. Article
  6. Review
  7. Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Agonist antibody to MuSK protects mice from MuSK myasthenia gravis.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  16. The MuSK agonist antibody protects the neuromuscular junction and extends the lifespan in C9orf72-ALS mice.Molecular therapy : the journal of the American Society of Gene Therapy · 2024
    Article
  17. Article
  18. Article
  19. Building, Breaking, and Repairing Neuromuscular Synapses.Cold Spring Harbor perspectives in biology · 2024
    Review
  20. Article

34 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

3 authors at 1 institution in 1 country.

Steven J BurdenMolecular Neurobiology Program, Helen L. and Martin S. Kimmel Center for Biology and Medicine at the Skirball Institute of Biomolecular Medicine, NYU Medical School, New York, NY 10016, USA.
Norihiro Yumoto
Wei Zhang
New York University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Muscle-specific kinase (MuSK) is essential for each step in neuromuscular synapse formation. Before innervation, MuSK initiates postsynaptic differentiation, priming the muscle for synapse formation. Approaching motor axons recognize the primed, or prepatterned, region of muscle, causing motor axons to stop growing and differentiate into specialized nerve terminals. MuSK controls presynaptic differentiation by causing the clustering of Lrp4, which functions as a direct retrograde signal for presynaptic differentiation. Developing synapses are stabilized by neuronal Agrin, which is released by motor nerve terminals and binds to Lrp4, a member of the low-density lipoprotein receptor family, stimulating further association between Lrp4 and MuSK and increasing MuSK kinase activity. In addition, MuSK phosphorylation is stimulated by an inside-out ligand, docking protein-7 (Dok-7), which is recruited to tyrosine-phosphorylated MuSK and increases MuSK kinase activity. Mutations in MuSK and in genes that function in the MuSK signaling pathway, including Dok-7, cause congenital myasthenia, and autoantibodies to MuSK, Lrp4, and acetylcholine receptors are responsible for myasthenia gravis.

Indexed as

AgrinCell DifferentiationHumansLDL-Receptor Related ProteinsModels, BiologicalMusclesMyasthenia GravisMyasthenic Syndromes, CongenitalProtein Structure, TertiaryReceptor Protein-Tyrosine KinasesReceptors, CholinergicSynapsesAgrinLDL-Receptor Related ProteinsLRP4 protein, humanMUSK protein, humanReceptor Protein-Tyrosine KinasesReceptors, Cholinergic

Identifiers

PMID23637281
PMCPMC3632064
OpenAlexW2123125411

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.