コーパス検索結果 (1語後でソート)
通し番号をクリックするとPubMedの該当ページを表示します
1 markers of neuromuscular dysfunction (CHRNA1/MUSK).
2 eceptor for muscle-specific tyrosine kinase (MuSK).
3 he muscle specific receptor tyrosine kinase (MUSK).
4 protein 4 (Lrp4) and muscle-specific kinase (MuSK).
5 he muscle-specific receptor tyrosine kinase (MuSK).
6 s have antibodies to muscle-specific kinase (MuSK).
7 AChR) or to muscle-specific tyrosine kinase (MuSK).
8 s to neural Agrin by binding and stimulating MuSK.
9 of how signals are transduced from agrin to MuSK.
10 ator to promote association between Lrp4 and MuSK.
11 eptide representing the Dok7-binding site on MuSK.
12 n essential intracellular binding protein of MuSK.
13 27V are both located in the kinase domain of MuSK.
14 ed uniformly in mice lacking either agrin or MuSK.
15 for proper folding of Ig1 and processing of MuSK.
16 ne complex is required for the activation of MuSK.
17 the membrane and formation of a complex with MuSK.
18 in that acts by binding to LRP4 to stimulate MuSK.
19 develop antibodies against agrin, LRP4, and MuSK.
21 itter receptor, (ii) muscle-specific kinase (MuSK), a receptor tyrosine kinase essential for the form
22 nction downstream of muscle-specific kinase (MuSK), a receptor tyrosine kinase expressed in skeletal
24 scle proteins: LRP4, the receptor for Agrin; MuSK, a receptor tyrosine kinase (RTK); and Dok7 (or Dok
25 uromuscular synapse formation by stimulating MuSK, a receptor tyrosine kinase expressed in skeletal m
30 rin, a factor released from motoneurons, and MuSK, a transmembrane tyrosine kinase that is activated
31 These papers substantially reshape the agrin-MuSK-ACh hypothesis of neuromuscular synaptogenesis.
32 surface LRP4 levels, inhibited agrin-induced MuSK activation and AChR clustering, and activated compl
35 e structure provides the molecular basis for MuSK activation by Dok7 and for rationalizing several Do
36 is responsible for transducing signals from MuSK activation to AChR clustering, culminating in cross
37 trate that Lrp4 is necessary, independent of MuSK activation, for presynaptic differentiation in vivo
45 and that the combinatorial function of UnpFL/MuSK and dystroglycan generates diverse patterns of vert
46 pathway, Tid1, which directly interacts with MuSK and is responsible for transducing signals from MuS
48 like domain of MuSK, prevent binding between MuSK and Lrp4, and inhibit Agrin-stimulated MuSK phospho
49 ceptor clusters, and increased expression of MuSK and Lrp4, two cell surface receptors required for N
50 to neuromuscular synapse formation, such as MuSK and nAChRs, are induced before muscle innervation o
54 napse formation by binding agrin, activating MuSK and stimulating postsynaptic differentiation, and f
55 ynapse formation can occur in the absence of MuSK and that the combinatorial function of UnpFL/MuSK a
58 e find that muscle-specific receptor kinase (MuSK) and its putative ligand Wnt11r are crucial for res
59 te the expression of muscle specific kinase (MuSK) and rapsyn (a cytoplasmic MuSK effector protein) i
60 immunosorbent assay and Western blot; AChR, MuSK, and anti-striated muscle antibodies were detected
61 Mutations have been identified in agrin, MuSK, and LRP4 in patients with congenital myasthenic sy
63 ce share similar mechanisms, requiring Lrp4, MuSK, and neuronal Agrin but not the MuSK Fz-like domain
64 te that Dok-7 also functions downstream from MuSK, and we identify the proteins that are recruited to
67 in neuromuscular transmission failure since MuSK antibodies alter neuromuscular junction morphology
69 her immune components, suggesting that these MuSK antibodies cause disease by directly interfering wi
71 imilar approach was used to demonstrate that MuSK antibodies, although mainly IgG4, were partially Ig
74 23.7%; P = .02), and 0 of 11 who had MG with MuSK antibodies; 0 of 29 controls had cortactin antibodi
75 , and in others anti-muscle-specific kinase (MuSK) antibodies that show pathogenic effects in vivo.
76 de studies confirm three major phenotypes in MuSK antibody positive myasthenia gravis (MMG) patients:
77 Antibodies to muscle specific kinase [MuSK; MuSK antibody positive myasthenia gravis (MuSK-MG)] make
79 certain how muscle specific tyrosine kinase (MuSK) antibody positive myasthenia gravis results in neu
80 reatment of muscle-specific tyrosine kinase (MuSK) antibody positive myasthenia gravis will be review
81 he muscle-specific receptor tyrosine kinase (MuSK) are essential for the acetylcholine receptor (AChR
82 linesterase, and the muscle-specific kinase, MuSK, are expressed selectively by a small number of myo
83 which bind the Frizzled (Fz)-like domain in MuSK, are required for prepatterning, suggesting that Wn
87 e we show that pathogenic IgG4 antibodies to MuSK bind to a structural epitope in the first Ig-like d
89 aveolin-3 is a novel muscle-specific kinase (MuSK) binding protein and that altered nAChR clustering
91 LDLR family member that forms a complex with MuSK, binds neural agrin and stimulates MuSK kinase acti
93 ted to RTKs, Dok7 is not only a substrate of MuSK, but also an activator of MuSK's kinase activity.
95 in cultured myotubes show that regulation of MuSK by PDZRN3 plays an important role in MuSK-mediated
97 dings demonstrate that missense mutations in MUSK can result in a severe form of CMS and indicate tha
98 method for the determination of 9 synthetic musk compounds in seafood products by combining the quic
103 inct species and it clarifies that Himalayan musk deer and Kashmir musk deer are confirmed instead of
104 arifies that Himalayan musk deer and Kashmir musk deer are confirmed instead of Alpine musk deer Mosc
105 nvestigated the phylogenetic relationship of musk deer from the central and western Himalayas based o
108 ir musk deer are confirmed instead of Alpine musk deer Moschus chrysogaster which has been previously
110 eer Mustang lineage was confirmed as Kashmir musk deer Moschus cupreus and has wide distribution in t
111 rom central Nepal are confirmed as Himalayan musk deer Moschus leucogaster and represent a species co
118 hat this prepatterning of AChRs, via a novel MuSK-dependent Wnt pathway, may guide motor axons to the
122 proteins that associate with the initiating MuSK/Dok-7/Crk/CrkL complex, regulate acetylcholine rece
123 e that appears independent of the Agrin-LRP4-MuSK-DOK7 acetylcholine receptor clustering pathway.
124 DOK7 is a component within the AGRN-LRP4-MUSK-DOK7 signalling pathway that is key for the formati
126 eta) expression, suggesting that the role of MuSK during memory consolidation critically involves the
128 that Wnt11r binds to the zebrafish unplugged/MuSK ectodomain to organize this central muscle zone.
129 ncoding either MuSK or rapsyn (a cytoplasmic MuSK effector protein) fused to green fluorescent protei
130 ific kinase (MuSK) and rapsyn (a cytoplasmic MuSK effector protein) in the tibialis anterior muscle o
131 leimide sensitive factor (NSF) in regulating MuSK endocytosis and subsequent signaling in response to
132 usk is prepatterned in muscle and that early Musk expression in developing myotubes is sufficient to
137 on source helped to distinguish two isomeric musk fragrances by means of different ionization behavio
139 , biocides, additives, corrosion inhibitors, musk fragrances, UV light stabilizers, and industrial ch
146 denervated muscle suppressed Mgn, nAChR, and MuSK gene induction, whereas Dach2 knockdown induced Mgn
152 Muscle-specific tyrosine kinase receptor (MuSK) has been believed to be mainly expressed and funct
154 he muscle-specific receptor tyrosine kinase, MuSK, have critical roles in synapse-specific transcript
155 hR) and a kinase critical for NMJ formation, MuSK; however, a proportion of MG patients are double-ne
159 ere, we demonstrate that the CRD deletion of MuSK in mice caused profound defects of both muscle prep
160 n that is thought to act in cis to stimulate MuSK in muscle fibers for postsynaptic differentiation.
163 emonstrating that the postsynaptic cell, and MuSK in particular, has a potent role in regulating the
164 ped procedure was applied to determine nitro musks in environmental water samples and was demonstrate
166 or the determination of synthetic polycyclic musks in oyster samples by using one-step microwave-assi
167 DEP), dibutyl phthalate (DBP), and synthetic musks in the gas phase and for DEHP, DiBP, DBP, and DINP
168 suggesting that association between Lrp4 and MuSK, independent of additional ligands, initiates prepa
169 e N-terminal half of Tid1 induced agrin- and MuSK-independent phosphorylation and clustering of AChRs
170 novel signaling pathway by which Agrin-LRP4-MuSK induces tyrosine phosphorylation of Rapsn, which is
183 ved for the two nitro musks (musk xylene and musk ketone) are significantly lower ranging between MDL
189 of MuSK by PDZRN3 plays an important role in MuSK-mediated nicotinic acetylcholine receptor clusterin
190 nteraction with the receptor tyrosine kinase MuSK, mediates accumulation of acetylcholine receptors (
192 vide insight into the unique pathogenesis of MuSK MG and provide clues toward development of specific
193 in mice have shown that IgG4 antibodies from MuSK MG patients cause disease without requiring complem
194 that the autoantigen drives autoimmunity in MuSK MG through the accumulation of somatic mutations su
196 areas with T1W high signal were increased in MuSK-MG patients and the intensity of the signal on axia
197 ) and orbicularis oculi (O.oculi) muscles in MuSK-MG patients compared with healthy controls, whereas
203 K; MuSK antibody positive myasthenia gravis (MuSK-MG)] make up a variable proportion of the remaining
204 sequencing of the BCR repertoire of AChR-MG, MuSK-MG, and healthy subjects to generate approximately
206 normalities were unique to either AChR-MG or MuSK-MG, indicating that the repertoires reflect the dis
207 cant muscle atrophy and fatty replacement in MuSK-MG, which was not found in the AChR-MG patients.
208 loping mammalian neuromuscular junction, but MuSK might also be protective in some neuromuscular dise
209 phosphorylates the receptor tyrosine kinase MuSK (muscle specific receptor tyrosine kinase) at the n
210 cle depends on the receptor tyrosine kinase, MuSK (muscle, skeletal receptor tyrosine-protein kinase)
212 tamination levels observed for the two nitro musks (musk xylene and musk ketone) are significantly lo
215 rm of CMS and indicate that the inability of MuSK mutants to interact with Dok-7, but not with Lrp4 o
219 cal analyses of MuSK mutants introduced into MuSK(-/-) myotubes demonstrate that residues in this hyd
220 tin biosensor we show that in the absence of MuSK neural crest cells fail to retract non-productive l
222 0 responds to macrocyclic ketone and lactone musk odorants but not to polycyclic musk odorants or a m
223 lactone musk odorants but not to polycyclic musk odorants or a macrocyclic diester musk odorant.
225 ion of a functional complex between Lrp4 and MuSK on the surface of myotubes in the absence of the tr
226 not form in their absence, and mutations in MuSK or downstream effectors are a major cause of a grou
227 eno-associated viral vectors encoding either MuSK or rapsyn (a cytoplasmic MuSK effector protein) fus
228 In mdx mice, enhanced expression of either MuSK or rapsyn ameliorated the acute loss of muscle forc
230 ine receptor (AChR), muscle-specific kinase (MuSK) or other AChR-related proteins in the postsynaptic
234 identification of a new player in the agrin-MuSK pathway, Tid1, which directly interacts with MuSK a
239 aromatic hydrocarbons (PAHs), and polycyclic musks (PCMs) were correlated with sources at a scale of
241 yotubes, the initial stages of agrin-induced MuSK phosphorylation and AChR clustering are normal, but
242 caused severe impairment of agrin-dependent MuSK phosphorylation, aggregation of acetylcholine recep
243 only moderate impairment of agrin-dependent MuSK phosphorylation, aggregation of AChRs and interacti
244 motor neuron-derived ligand that stimulates MuSK phosphorylation, play critical roles in synaptic di
245 rin, which binds Lrp4 and stimulates further MuSK phosphorylation, stabilizing nascent synapses.
248 tural epitope in the first Ig-like domain of MuSK, prevent binding between MuSK and Lrp4, and inhibit
249 wever, clustering of muscle specific kinase (MuSK) proceeded normally in the gamma-null muscles.
250 pic interactions to mediate co-clustering of MuSK, rapsyn, and acetylcholine receptors at the NMJ.
252 lized by motor neurons to stimulate the LRP4-MuSK receptor in muscles for neuromuscular junction (NMJ
254 propose that Wnt-induced trafficking of the MuSK receptor to endosomes initiates a signaling cascade
260 species termed crowned shrew HBV (CSHBV) and musk shrew HBV (MSHBV), each containing distinct genotyp
264 a coreceptor of agrin that is necessary for MuSK signaling and AChR clustering and identify a potent
265 te AChR clustering by facilitating the agrin/MuSK signaling and the interaction between the receptor
266 ults provide new insight into the agrin-LRP4-MuSK signaling cascade and NMJ formation and represent a
268 Its expression enables agrin binding and MuSK signaling in cells that otherwise do not respond to
269 propose that Wnt ligands activate unplugged/MuSK signaling in muscle fibers to restrict growth cone
272 aptic differentiation are dependent on Agrin/MuSK signaling without a requirement for a secondary sig
274 synaptic effects, suggesting novel roles for MuSK signalling in muscle physiology and pathophysiology
276 Pathogenic muscle-specific tyrosine kinase (MuSK)-specific IgG4 autoantibodies in autoimmune myasthe
277 ral lines of evidence suggest that agrin and MuSK stimulate synapse-specific transcription indirectly
280 of muscle-specific receptor tyrosine kinase (MuSK), the key organizer of postsynaptic development at
281 ndent of the muscle-specific tyrosine kinase MuSK, the known binding partner of Dok-7 at the NMJ.
285 synaptic acetyl-choline receptor (nAChR) and MUSK transcription whereas forced expression of HDAC4 mi
287 show that in vivo, wnt11r and wnt4a initiate MuSK translocation from muscle membranes to recycling en
288 nockdown of several core components disrupts MuSK translocation to endosomes, AChR localization and a
289 ells attenuates agrin binding, agrin-induced MuSK tyrosine phosphorylation, and AChR clustering.
293 suggest that Lrp4 is a cis-acting ligand for MuSK, whereas Agrin functions as an allosteric and parac
294 ential for activation of the receptor kinase MuSK, which governs NMJ formation, and DOK7 mutations un
295 demonstrate that the first Ig-like domain in MuSK, which shares homology with the NGF-binding region
296 choline receptors (AChRs) and interaction of MuSK with Dok-7, an essential intracellular binding prot
299 ion levels observed for the two nitro musks (musk xylene and musk ketone) are significantly lower ran