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prepatterning in zebrafish requires the MuSK Fz-like domain but not Lrp4 (show LRP4 Proteins)
Data show that in vivo, wnt11r (show WNT11 Proteins) and wnt4a initiate MuSK translocation from muscle membranes to recycling endosomes and that this transition is crucial for AChR accumulation at future synaptic sites.
Data suggest that a Wnt11r (show WNT11 Proteins)-MuSK dependent, PCP (show PRCP Proteins)-like pathway restricts neural crest cells to their segmental path.
AChR prepatterning and axonal guidance are spatio-temporally coordinated through common unplugged/MuSK signals, and that additional factor(s) restrict unplugged/MuSK signaling to a central muscle zone critical for establishing mid-muscle synaptogenesis
Zebrafish unplugged encodes a homolog of muscle-specific (show EIF3K Proteins) kinase (MuSK); unlike mammalian MuSK, unplugged has only a limited role in neuromuscular synaptogenesis.
genetic evidence that neuromuscular synapse formation can occur in the absence of MuSK and that the combinatorial function of UnpFL/MuSK and dystroglycan generates diverse patterns of vertebrate neuromuscular innervation.
These mice showed only marginal activation of MuSK and died by 3 weeks of age apparently due to an abnormally small number and size of neuromuscular junction (NMJs).
data reveal that muscle skeletal receptor tyrosine kinase cysteine-rich domain is critical for neuromuscular junction formation and plays an unsuspected role in NMJ maintenance in adulthood.
Forced expression of Dok-7 (show DOK7 Proteins) in muscle enhanced MuSK activation in mice lacking agrin (show AGRN Proteins) or Lrp4 (show CORIN Proteins) and restored midmuscle NMJ formation in agrin (show AGRN Proteins)-deficient mice, but not in Lrp4 (show CORIN Proteins)-deficient mice.
pathogenic IgG4 antibodies to MuSK bind to a structural epitope in the first Ig-like domain of MuSK, prevent binding between MuSK and Lrp4 (show CORIN Proteins), and inhibit Agrin (show AGRN Proteins)-stimulated MuSK phosphorylation.
MuSK colocalizes with actin and Arf6 (show ARF6 Proteins) at the cell surface and during endosomal trafficking.
Increasing MuSK activity delays denervation and improves motor function in ALS mice.
Two classic synaptic signalling systems (neuregulin-1 (show NRG1 Proteins) and neural agrin (show AGRN Proteins)) converge upon MuSK to regulate postsynaptic differentiation.
Biglycan (show BGN Proteins) binding to MuSK rescues the unstable acetylcholine receptor (show CHRNB1 Proteins) clusters that are involved in neuromuscular junction formation and postsynaptic differentiation.
Data suggest that adult skeletal muscles harbour different endogenous levels of MuSK and that these levels determine the ability to form ectopic AChR clusters upon overexpression of agrin (show AGRN Proteins) or MuSK.
Depletion of MuSK at the neuromuscular junction leads to disassembly of muscle-specific (show EIF3K Proteins) kinase and muscle weakness of myasthenia gravis in mice.
Classical electromyography revealed the presence of myopathic changes more frequently in MuSK myasthenia gravis compared to acetylcholine receptor (show CHRNA1 Proteins) myasthenia gravis
A Dutch founder mutation in MUSK causing fetal akinesia deformation sequence has been found in 14 fetuses.
To our knowledge, this is the first report showing that a mutation in MuSK is associated with Fetal akinesia deformation sequence syndrome
Immunosuppression attenuates the Th1 (show TH1L Proteins) response in AChR-myasthenia gravis (MG) and MuSK-MG, but otherwise modulates immune responses in AChR-MG and MuSK-MG patients differentially.
HnRNP C, YB-1 (show YBX1 Proteins) and hnRNP L (show HNRNPL Proteins) coordinately enhance skipping of human MUSK exon 10 to generate a Wnt (show WNT2 Proteins)-insensitive MuSK isoform.
MuSK myasthenia gravis IgG4 disrupts the interaction of LRP4 (show LRP4 Proteins) with MuSK but both IgG4 and IgG1-3 can disperse preformed agrin (show AGRN Proteins)-independent AChR clusters
[review] Recent discovery of two novel target proteins (MuSK and LRP4 (show LRP4 Proteins)) has reduced the percentage of patients without known autoantibodies, although there are still some seronegative myasthenia gravis patients.
Identification of a novel missense mutation c.114T > A; p.Asp38Glu heteroallelic to a genomic deletion encompassing exons 2-3 of MUSK that explain a limb-girdle congenital myasthenic syndrome in two affected brothers of a Turkish family.
HEp (show EPHB6 Proteins)-2 M4 cells revealed a high specificity for the detection of MuSK autoantibodies from 25 patient sera.
This study provides a replication of the highly significant associations of both HLA-DRB1 (show HLA-DRB1 Proteins)( *)16,-DRB1 (show RBM45 Proteins)( *)14 and -DQB1( *)05 with MuSK-MG.
This gene encodes a muscle-specific tyrosine kinase receptor. The encoded protein may play a role in clustering of the acetylcholine receptor in the postsynaptic neuromuscular junction. Mutations in this gene have been associated with congenital myasthenic syndrome. Alternatively spliced transcript variants have been described.
muscle, skeletal receptor tyrosine-protein kinase
, muscle, skeletal, receptor tyrosine kinase
, skeletal muscle receptor tyrosine kinase
, muscle, skeletal receptor tyrosine-protein kinase-like
, muscle localized kinase 2
, muscle, skeletal receptor tyrosine protein kinase
, muscle-specific kinase receptor
, muscle-specific protein kinase secretory isoform
, muscle-specific tyrosine protein kinase receptor
, muscle-specific tyrosine-protein kinase receptor
, muscle specific kinase (neural fold/somite kinase 1)
, muscle-specific tyrosine kinase receptor MuSK
, skeletal receptor tyrosine protein kinase