ライフサイエンスコーパス: AChR

1 AChR clusters became fragmented with diminished junction

2 AChR clusters were almost equally distributed between Lo

3 AChR internalized via small vesicles having lower GP and

4 AChR-MG and MuSK-MG subjects displayed distinct gene seg

5 AChRs might provide a valuable proxy to decipher the fun

6 e agonist's quaternary ammonium (QA) and (2) AChRs respond strongly to ACh because an H-bond position

7 mutant receptor (M(3)-AChR-N514Y) using M(3)-AChR constructs that report receptor activation by chang

8 q)-coupled M(3) acetylcholine receptor (M(3)-AChR) with that of a constitutively active mutant recept

9 centrations, the activation kinetics of M(3)-AChR-N514Y were significantly faster, whereas at maximal

10 constitutively active mutant receptor (M(3)-AChR-N514Y) using M(3)-AChR constructs that report recep

11 se for acetylcholine and carbachol with M(3)-AChR-N514Y.

12 nteraction was measured by FRET between M(3)-AChR-yellow fluorescent protein (YFP) and cyan fluoresce

13 ased visual screen for mutants with abnormal AChR distribution, we isolated the ras suppressor 1 (rsu

14 neurotransmitter receptor for acetylcholine (AChR) display a series of cholesterol consensus domains

15 ler and less voltage-dependent than in adult AChRs.

16 AChR) response in MG, MHC class II and alpha-AChR subunit as well as chemokines involved in GC develo

17 sduction pathway altered MHC Class II, alpha-AChR, and CXCL13 expression.

18 that estrogens inhibited expression of alpha-AChR and HLA-DR in TECs, suggesting that estrogens may a

19 receptor agonists on the expression of alpha-AChR and various tissue-specific antigens (TSAs) in huma

20 fically triggers the overexpression of alpha-AChR in TECs and not of other TSAs.

21 ifically increase thymic expression of alpha-AChR in wild-type mice, but not in IFN-I receptor knocko

22 d RNA (dsRNA), stimulated specifically alpha-AChR expression, the signaling pathways involved were in

23 ta (gamma-AChRs) and alpha1beta1epsilondelta AChRs (epsilon-AChRs) in Xenopus oocytes revealed that P

24 of the M1-M2 linker cysteines of the alpha3 AChR subunit.

25 etylcholine receptor (AChR), the alpha3beta4 AChR and the homomeric alpha1 glycine receptor (GlyR).

26 r subsynaptic accumulations of ACR-16/alpha7 AChRs, a consequent reduction in synaptic current, and p

27 control the timing of AChR expression in an AChR-less fish background.

28 inhibited agrin-induced MuSK activation and AChR clustering, and activated complements, revealing po

29 utant CLASP2 in clusters, but MT capture and AChR cluster size are reduced.

30 ad ocular MG at onset than those with MG and AChR antibodies, although the difference was not statist

31 t the clusters) had little effect on aneural AChR clusters at E13.5, suggesting that SCs may not be n

32 These injections also lead to an anti-AChR autoimmune response characterized by a significant

33 ensing molecules could contribute to an anti-AChR response.

34 Because anti-AChR antibodies are highly specific for MG and are patho

35 of MG patients are double-negative for anti-AChR and anti-MuSK antibodies.

36 was used in combination with monoclonal anti-AChR antibody labeling of live cells, which induces AChR

37 subsequently induced with a low dose of anti-AChR monoclonal antibody 35.

38 alues were normalized to a pretreatment anti-AChR antibody level of 100% and the mean levels after ea

39 ed by a significant production of serum anti-AChR antibodies and a specific proliferation of B cells.

40 ll responses, decreased levels of serum anti-AChR IgGs, and reduced complement activation at the neur

41 d that V188M markedly decreased the apparent AChR channel opening rate and gating efficiency.

42 at regulate surface trafficking of assembled AChR and may help prevent surface expression of unassemb

43 ns increased the surface levels of assembled AChR expressed in HEK cells to 138% of wild-type levels.

44 linked immunosorbent assay and Western blot; AChR, MuSK, and anti-striated muscle antibodies were det

45 and cytokine production in response to both AChR and control Ags were measured from 3120 T cell libr

46 hronically denervated muscles, in which both AChR stability and recycling are significantly decreased

47 We found plectin isoform 1f (P1f) to bridge AChRs and IFs via direct interaction with the AChR-scaff

48 tions differentiate as in the wild type, but AChRs assemble into ectopic clusters that progressively

49 excessive growth of motor axons that bypass AChR clusters.

50 s in the neuromuscular ACh receptor channel (AChR) to promote a reversible, global change in protein

51 Acetylcholine receptor-channels (AChRs) mediate fast synaptic transmission between nerve

52 These observations also apply to the classic AChR MG phenotype seen in large series.

53 The clustered AChR CBA detected antibodies in 38.1% (16 of 42) of RIPA

54 Patients with antibodies only to clustered AChRs appear to be younger and have milder disease than

55 , patients with antibodies only to clustered AChRs had frequent prepubertal onset (62.5% [median age,

56 AChR antibodies and antibodies to clustered AChRs in 138 patients.

57 ents were tested for antibodies to clustered AChRs, and 42 had a final diagnosis of MG.

58 tin-deficient cells rescued both compromised AChR clustering and IF network anchoring.

59 In contrast, AChRs did not recycle at agrin-induced clusters in C2C12

60 f post-transcriptional events in controlling AChR expression in skeletal muscle, and points toward a

61 ing to the plasma membrane and not decreased AChR turnover.

62 significantly altered as a result of delayed AChR expression.

63 t cholesterol analog fPEG-cholesterol, i.e., AChR endocytosis was essentially dissociated from that o

64 Each AChR has two neurotransmitter binding sites located at t

65 rticular abnormalities were unique to either AChR-MG or MuSK-MG, indicating that the repertoires refl

66 Importantly, HuR binds to endogenous AChR beta-subunit transcripts in cultured myotubes and i

67 ts disrupts MuSK translocation to endosomes, AChR localization and axonal guidance.

68 1 transmembrane helix of the muscle endplate AChR is linked to a beta-strand of the extracellular dom

69 utations would suggest that reduced endplate AChR due to defective N-linked glycosylation is a primar

70 hus, it is possible to forecast and engineer AChR responses simply by combining perturbations.

71 fiber growth; (2) a defective gamma/epsilon-AChR subunit switch, preferentially at synapses on slow

72 ) and alpha1beta1epsilondelta AChRs (epsilon-AChRs) in Xenopus oocytes revealed that PEA selectively

73 ected the rundown of ACh currents in epsilon-AChRs.

74 t, does not require rapsyn because expressed AChRs are visible on the cell membranes of rapsyn-defici

75 affinity, and detected the presence of fetal AChR on a number of rhabdomyosarcoma cell lines.

76 However, mAb 131 did not reduce fetal AChR ion channel currents in electrophysiological experi

77 specific for the gamma-subunit of the fetal AChR to which it bound with sub-nanomolar apparent affin

78 lpha-bungarotoxin binding sites on the fetal AChR, and partially blocked the binding of an antibody (

79 behave independently in both adult and fetal AChRs.

80 to exchange function between adult and fetal AChRs.

81 The gamma-subunit of fetal AChRs is indispensable for the proper development of neu

82 Synaptic sites with fetal AChRs in weanling muscle were ~3% in control and ~40% in

83 omes and that this transition is crucial for AChR accumulation at future synaptic sites.

84 neuron innervation determined the sites for AChR clustering, a complete reversal of normal neuromusc

85 t LRP4 is involved in deciding where to form AChR clusters in muscle fibers, postsynaptic differentia

86 We show that at nerve-free AChR clusters induced by agrin in extrasynaptic membrane

87 aled that rapsyn self-clusters separate from AChRs did not exist before synapse formation.

88 man recombinant alpha1beta1gammadelta (gamma-AChRs) and alpha1beta1epsilondelta AChRs (epsilon-AChRs)

89 first report of an association between high AChR antibody levels and progression from OMG to general

90 ially expressed cytoplasmic domains of human AChR subunits reduced the development of chronic EAMG in

91 onal EMC members in C. elegans also impaired AChR synthesis and induced the unfolded protein response

92 h events cannot fully account for changes in AChR expression following denervation.

93 tiation associated with a drastic deficit in AChR clusters and excessive growth of motor axons that b

94 density, suggesting that SCs are involved in AChR cluster maturation.

95 A reduction in AChR protein was documented in line with the above mRNA

96 ppears that all of the intermediate steps in AChR activation comprise a single, energetically coupled

97 e dependence of alphaArg209 on alphaGlu45 in AChRs from different species, and compare the full agoni

98 romotes MT capture at clusters and increases AChR cluster size, compared with myotubes that express s

99 otubes cultured on agrin patches that induce AChR clustering in a two-dimensional manner.

100 ld protein, serves as an E3 ligase to induce AChR clustering and NMJ formation, possibly by regulatio

101 serve as agrin's receptor in trans to induce AChR clusters.

102 ty inhibits rapsyn- as well as agrin-induced AChR clustering in heterologous and muscle cells.

103 and focal vesicle delivery to agrin-induced AChR clusters are also inhibited by microtubule- and act

104 ASP2 regulates AChR density at agrin-induced AChR clusters in cultured myotubes via PI3 kinase acting

105 ssociated with or devoid of antibody-induced AChR clusters, respectively.

106 resulted in smaller and fewer nerve-induced AChR clusters; however, SC ablation at E15.5 reduced ACh

107 tibody labeling of live cells, which induces AChR clustering.

108 established EAMG, and that the MDSCs inhibit AChR-specific immune responses at least partially in an

109 grin in extrasynaptic membrane, internalized AChRs are driven back into the ectopic synaptic clusters

110 s by promoting the recycling of internalized AChRs, which would otherwise be destined for degradation

111 eveals that L1 muscle cells express a main L-AChR type composed of five different subunits: UNC-38, U

112 e absence of the alpha-type ACR-8 subunit, L-AChR channel properties are not modified, thus indicatin

113 nents of adult levamisole-sensitive AChRs (L-AChRs).

114 LEV-8 subunit is a component of native L1 L-AChRs but behaves as a nonessential subunit.

115 cating that ACR-8 is not a component of L1 L-AChRs.

116 Docking into homology modeled L-AChRs proposes that ACh forms the typical cation-pi inte

117 amisole-sensitive acetylcholine receptors (L-AChRs) requires the muscle-secreted scaffolding protein

118 in (SST) interneurons in the mPFC express M1-AChR at higher levels than parvalbumin interneurons.

119 MKII+) interneurons in the mPFC expressed M1-AChR.

120 Moreover, knockdown of M1-AChR in SST interneurons in the mPFC demonstrated that M

121 In mice, viral-mediated knockdown of M1-AChR specifically in GABAergic neurons, but not glutamat

122 -type muscarinic acetylcholine receptors (M1-AChR); however, the cellular mechanisms underlying activ

123 nterneurons in the mPFC demonstrated that M1-AChR expression in these neurons is required for the rap

124 eplace GAA to the affected tissue and modify AChR mRNA expression, muscle force production, motor end

125 unculin A had the opposite effect, with more AChR clusters associated with Lo domains.

126 rong interdependence in both human and mouse AChRs, whereas the functional consequences of the mutati

127 from single channel currents of fetal mouse AChRs expressed in tissue-cultured cells.

128 these and other agonists in adult-type mouse AChRs having a mutation(s) at the transmitter-binding si

129 ons in rats do express Gq-coupled muscarinic AChRs, which appear to have gone undetected in the previ

130 ely express pirenzepine-sensitive muscarinic AChRs.

131 mary visual cortex astrocytes via muscarinic AChRs.

132 y validated model of the open-channel muscle AChR.

133 oteins consisting of CD4 fused to the muscle AChR subunit cytoplasmic loops.

134 New AChR clustering is also induced by axon terminals that f

135 n a Golgi-based regulatory step in nicotinic AChR trafficking.

136 he repetitive activation of muscle nicotinic AChRs.

137 and glutamate synaptic release via nicotinic AChRs.

138 otato revealed that rapsyn in the absence of AChR was localized in the Golgi complex.

139 R mRNAs due to transcriptional activation of AChR subunit genes.

140 The memory compartment of AChR-MG was further characterized by reduced positive se

141 NA significantly enhanced the degradation of AChR alpha-subunits (AChRalpha), leading to fewer and sm

142 CLASP2, and LL5beta, for precise delivery of AChR vesicles from the subsynaptic nuclei to the overlyi

143 , increases the size and receptor density of AChR clusters at the NMJ through the delivery of AChRs a

144 In conclusion, the distribution of AChR submicron-sized clusters at the cell membrane appea

145 t muscle denervation increases expression of AChR mRNAs due to transcriptional activation of AChR sub

146 The extent of AChR recycling depended on the strength of the agrin sti

147 l systems in MT capture and in the fusion of AChR vesicles with the cluster membrane.

148 in the literature about the implications of AChR antibody levels and progression from OMG to general

149 With the delayed induction of AChR expression after an extensive period of AChR-less d

150 his is due to reduced steady-state levels of AChR alpha, delta, epsilon, but not beta subunits rather

151 e also involved in controlling the levels of AChR mRNAs following denervation.

152 bility assays revealed that the half-life of AChR beta-subunit mRNAs was increased in the presence of

153 of CLASP2 play a role in the maintenance of AChR cluster size through the regulated capture and rele

154 is crucial for formation and maintenance of AChR clusters, postsynaptic NMJ organization, and body l

155 Despite the accepted model of AChR regulation, which implicates transcriptional mechan

156 rane mean di-4-ANEPPDHQ GP and the number of AChR clusters associated with Ld membrane domains increa

157 AChR expression after an extensive period of AChR-less development, paralyzed fish displayed a remark

158 However, in the presence of AChR subunits, rapsyn molecules were targeted to the cel

159 l legs, which correlated with a reduction of AChR protein levels at the neuromuscular junction (appro

160 and NMJ formation, possibly by regulation of AChR neddylation.

161 med deep sequencing of the BCR repertoire of AChR-MG, MuSK-MG, and healthy subjects to generate appro

162 ne characteristics, OMG symptoms, results of AChR antibody testing, and progression time to generaliz

163 We demonstrate a higher sensitivity of AChR antibody testing than previously reported in the la

164 at the NMJ and how this controls the size of AChR clusters are not yet understood.

165 , the density of synaptic AChRs, the size of AChR clusters, and the numbers of subsynaptic muscle nuc

166 turn, causes an increase in the stability of AChR beta-subunit mRNAs in denervated muscle.

167 y leading to an increase in the stability of AChR beta-subunit transcripts.

168 in which we can freely control the timing of AChR expression in an AChR-less fish background.

169 ubunits rather than altered transcription of AChR-subunit RNA.

170 (ARE) in the 3'-untranslated region (UTR) of AChR beta-subunit mRNA.

171 ase and consequently for dense clustering of AChRs, we hypothesized that reduced levels of Dok-7 incr

172 As a consequence, the synaptic content of AChRs is reduced.

173 clusters at the NMJ through the delivery of AChRs and that this is regulated by a pathway involving

174 chanisms that underlie the focal delivery of AChRs to the adult NMJ are not yet understood in detail.

175 ulate the metabolic stability and density of AChRs by promoting the recycling of internalized AChRs,

176 in vivo reduces the density and insertion of AChRs into the postsynaptic membrane.

177 ubes, neural agrin promotes the recycling of AChRs and thereby increases their metabolic stability.

178 sults provide evidence for an active role of AChRs in the targeting of rapsyn to the NMJ in vivo SIGN

179 llular factors required for the synthesis of AChRs, we performed a genetic screen in the nematode Cae

180 In contrast, the targeting of AChRs to the cell membrane does not require rapsyn.

181 The targeting of AChRs to the cell membrane, in contrast, does not requir

182 atellite cells (Pax7-Cre/cKO), uncoupling of AChRs from IFs was shown to lead to loss of postsynaptic

183 sense mutations have a deleterious effect on AChR clustering.

184 Among the 223 participants, AChR antibody testing results were positive in 158 parti

185 cetylcholine receptor autoantibody-positive (AChR+) generalized MG.

186 impaired synaptic structure as postsynaptic AChR clusters and their associated postsynaptic scaffold

187 m in response to the absence of postsynaptic AChRs, may underlie symptoms of neuromuscular diseases c

188 Postsynaptically, AChR clusters in HSA-beta-cat(flox(ex3)/+) diaphragms we

189 in mice lead nerve terminals to prepatterned AChRs.

190 pening rate constant) and sometimes produced AChRs that had heterogeneous gating kinetic properties.

191 durability of response and/or relapse rate, AChR autoantibody levels, adverse effects, and inflammat

192 toantibodies against acetylcholine receptor (AChR) and a kinase critical for NMJ formation, MuSK; how

193 ction, primarily the acetylcholine receptor (AChR) and the muscle-specific kinase.

194 improve detection of acetylcholine receptor (AChR) antibodies in patients with myasthenia gravis (MG)

195 iated mainly by anti-acetylcholine receptor (AChR) antibodies.

196 The sensitivity of acetylcholine receptor (AChR) antibody testing is thought to be lower in ocular

197 hat govern nicotinic acetylcholine receptor (AChR) assembly and trafficking are poorly defined, and t

198 g of the muscle-type acetylcholine receptor (AChR) channel depends on communication between the ACh-b

199 romuscular nicotinic acetylcholine receptor (AChR) channel gating have been measured by using single-

200 ich is essential for acetylcholine receptor (AChR) clustering and NMJ (neuromuscular junction) format

201 egions and performed acetylcholine receptor (AChR) clustering assays and used exon trapping to determ

202 12 cell line reduced acetylcholine receptor (AChR) clustering during myotube differentiation.

203 kL complex, regulate acetylcholine receptor (AChR) clustering in vitro, and are localized at synapses

204 reases agrin-induced acetylcholine receptor (AChR) clustering.

205 uronal agrin-induced acetylcholine receptor (AChR) clustering.

206 ibution of nicotinic acetylcholine receptor (AChR) clusters at the cell membrane was studied in CHO-K

207 rol the stability of acetylcholine receptor (AChR) clusters on the surface of cultured myotubes.

208 les at agrin-induced acetylcholine receptor (AChR) clusters, mediated to a large extent by the microt

209 he expression of the acetylcholine receptor (AChR) epsilon subunit gene mRNA in both muscles.

210 A muscle acetylcholine receptor (AChR) has two neurotransmitter binding sites located in

211 ies to the nicotinic acetylcholine receptor (AChR) or to muscle-specific tyrosine kinase (MuSK).

212 nes involved in anti-acetylcholine receptor (AChR) response in MG, MHC class II and alpha-AChR subuni

213 ed expression of the acetylcholine receptor (AChR) subunit, ACR-12::GFP.

214 e human adult-muscle acetylcholine receptor (AChR), the alpha3beta4 AChR and the homomeric alpha1 gly

215 the muscle nicotinic acetylcholine receptor (AChR), we have recently hypothesized that the conformati

216 ce showed suppressed acetylcholine receptor (AChR)-specific T cell responses, decreased levels of ser

217 directed toward the acetylcholine receptor (AChR).

218 bodies targeting the acetylcholine receptor (AChR-MG) or muscle specific kinase (MuSK-MG).

219 ter agrin removal and enhanced ACh receptor (AChR) cluster formation, but no change in cell number, e

220 contains seven different nicotinic receptor (AChR) subunits, five of which have been shown to be comp

221 aused by defects in ace-tylcholine receptor (AChR) function.

222 e the clustering of acetylcholine receptors (AChRs) and increase their metabolic stability in the mus

223 Acetylcholine receptors (AChRs) are heteromeric membrane proteins essential for n

224 ) traps and anchors acetylcholine receptors (AChRs) at high density at the synapse.

225 The accumulation of acetylcholine receptors (AChRs) at nerve terminals is critical for signal transmi

226 r the clustering of acetylcholine receptors (AChRs) at postsynaptic sites.

227 r the clustering of acetylcholine receptors (AChRs) at synaptic sites between mammalian motor neurons

228 Neuromuscular acetylcholine receptors (AChRs) have two transmitter binding sites: at alpha-delt

229 construct endplate acetylcholine receptors (AChRs) having only one functional neurotransmitter-bindi

230 ion of postsynaptic acetylcholine receptors (AChRs) impacts presynaptic release by establishing a gen

231 on of extrasynaptic acetylcholine receptors (AChRs) in Caenorhabditis elegans muscle cells.

232 Live imaging of acetylcholine receptors (AChRs) in cultured myotubes differentiated ex vivo from

233 ts in expression of acetylcholine receptors (AChRs) in skeletal muscle that occur even in the absence

234 the high density of acetylcholine receptors (AChRs) in the postsynaptic muscle membrane.

235 Nicotinic acetylcholine receptors (AChRs) mediate signaling in the central and peripheral n

236 dult-type nicotinic acetylcholine receptors (AChRs) mediate signalling at mature neuromuscular juncti

237 number of nicotinic acetylcholine receptors (AChRs) present in the plasma membrane of muscle and neur

238 Nicotinic acetylcholine receptors (AChRs) switch on/off to generate transient membrane curr

239 to muscle nicotinic acetylcholine receptors (AChRs) that impair neuromuscular transmission, thereby c

240 ion of one class of acetylcholine receptors (AChRs) to synapses.

241 es and postsynaptic acetylcholine receptors (AChRs) to the center of skeletal muscle cells.

242 rough activation of acetylcholine receptors (AChRs), (2) enhances glutamatergic synaptic transmission

243 unction, especially acetylcholine receptors (AChRs).

244 e redistribution of acetylcholine receptors (AChRs).

245 abilizing nicotinic acetylcholine receptors (AChRs).

246 the distribution of acetylcholine receptors (AChRs).

247 out the function of different ACh receptors (AChRs).

248 dly to choline (Cho), so endplate receptors (AChRs) are exposed to high concentrations of both of the

249 dly to choline (Cho), so endplate receptors (AChRs) are exposed to high concentrations of both of the

250 porter (VAChT, SLC18A3), and nACh receptors (AChRs, CHRNAs).

251 adult-type muscle mouse nicotinic receptors (AChRs) having mutations of agonist binding site amino ac

252 ity, agrin maintained the amount of recycled AChRs at agrin-induced clusters at a level similar to th

253 sters; however, SC ablation at E15.5 reduced AChR cluster size but had no effect on cluster density,

254 of GFPT1 expression both resulted in reduced AChR cell-surface expression.

255 romuscular diseases characterized by reduced AChRs, such as myasthenia gravis.

256 effective option in patients with refractory AChR+ MG, who were observed to have a durable response a

257 post-transcriptional events indeed regulate AChR beta-subunit mRNAs in response to denervation.

258 e plus end-tracking protein CLASP2 regulates AChR density at agrin-induced AChR clusters in cultured

259 of post-transcriptional events in regulating AChR beta-subunit mRNAs and point toward a central role

260 ibility to passive transfer MG, by rendering AChR clusters less resistant to the autoantibody attack.

261 enin GOF disrupted the signal that restricts AChR clustering to the middle region of muscle fibers.

262 be components of adult levamisole-sensitive AChRs (L-AChRs).

263 pression of heteromeric levamisole-sensitive AChRs by destabilizing unassembled subunits in the ER.

264 e expression of homomeric nicotine-sensitive AChRs and GABAA receptors in C. elegans muscle cells.

265 ts (AChRalpha), leading to fewer and smaller AChR clusters on the surface of differentiated C2C12 myo

266 genita which can be caused by fetal-specific AChR-blocking autoantibodies.

267 RIPA) and CBA were used to test for standard AChR antibodies and antibodies to clustered AChRs in 138

268 owed a significant reduction in cell-surface AChR expression (Pt1 P < 0.0001; Pt2 P = 0.0097).

269 The G74C mutation markedly reduced surface AChR expression in cultured cells, whereas the V188M mut

270 tic muscle membrane, the density of synaptic AChRs, the size of AChR clusters, and the numbers of sub

271 n vivo experiments with fluorescently tagged AChR or rapsyn in zebrafish larvae revealed that rapsyn

272 We conclude that AChRs enable the transport of rapsyn from the Golgi comp

273 These results indicate that AChRs play a critical role in the insertion and/or assoc

274 Previous studies suggest that AChRs might direct rapsyn self-clusters to the synapse.

275 luciferase reporter construct containing the AChR beta-subunit 3'UTR, caused an increase in luciferas

276 However, when the coiled-coil domain (the AChR-binding domain of rapsyn) is deleted, rapsyn fails

277 e amount of energy that is available for the AChR conformational change provided by different, struct

278 Examination of rapsyn in the AChR-less mutant sofa potato revealed that rapsyn in the

279 es have shown that the alpha2-subunit of the AChR (Chrna2) is expressed in the basal forebrain, in th

280 mutations in the extracellular domain of the AChR alpha subunit (AChRalpha) in a patient with myasthe

281 to maintain the structural integrity of the AChR assembly at the E-T interface.

282 None of the AChR kink mutations had a measureable effect on agonist

283 Some of the AChR loss that follows denervation is correlated with fa

284 y conduction-catalyzing conformations of the AChR's selectivity-filter glutamates.

285 tibody (mAb 637) to the alpha-subunit of the AChR, suggesting that both antibodies bind at or near on

286 Upon cholesterol depletion, only 12% of the AChR-containing vesicles costained with the fluorescent

287 ChRs and IFs via direct interaction with the AChR-scaffolding protein rapsyn in an isoform-specific m

288 of both IFN-gamma and IL-17, in response to AChR, was also restricted to the CCR6(+) memory T cell c

289 rom MG patients proliferating in response to AChR-derived peptides was significantly higher than that

290 traightening of the M1 proline kink triggers AChR desensitization.

291 ature neuromuscular junctions and fetal-type AChRs are necessary for proper synapse development.

292 uromuscular junction (NMJ) development where AChR clustering precedes innervation.

293 In cultured myoblasts (in which AChRs are absent), myristoylated WT rapsyn mostly locali

294 Immunization with AChR cytoplasmic domains in adjuvant is promising as a s

295 had dSNMG, 19 of 201 (9.5%) who had MG with AChR antibodies (significantly lower than those with dSN

296 8 (15.2%) had dSNMG, 201 (80.4%) had MG with AChR antibodies, and 11 (4.4%) had MG with MuSK antibodi

297 ibodies, compared with those who had MG with AChR antibodies, more frequently had mild forms at onset

298 case series study included 16 patients with AChR+ MG referred to an MG clinic from January 1, 2007,

299 the cell surface and formed aggregates with AChRs.

300 ) is deleted, rapsyn fails to associate with AChRs at NMJs of living mice.

301 to the cell surface via its interaction with AChRs.