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1 gate the association of the alpha5 nicotinic acetylcholine receptor.
2 t activity of NS6740 at the alpha7 nicotinic acetylcholine receptor.
3 elicit protean agonism at the muscarinic M2 acetylcholine receptor.
4 uscular junction proteins, in particular the acetylcholine receptor.
5 to target the human alpha9alpha10 nicotinic acetylcholine receptor.
6 lic analogue and the alpha9alpha10 nicotinic acetylcholine receptor.
7 ction is mediated by TRPA1 and not nicotinic acetylcholine receptors.
8 ty and was attenuated by blocking muscarinic acetylcholine receptors.
9 where it regulates the function of nicotinic acetylcholine receptors.
10 of the peptide and involved alpha7 nicotinic acetylcholine receptors.
11 eting the cannabinoid 1 and alpha7 nicotinic acetylcholine receptors.
12 an be rescued by an antagonist of muscarinic acetylcholine receptors.
13 mine neuron axons by activation of nicotinic acetylcholine receptors.
14 tein-coupled receptors, including muscarinic acetylcholine receptors.
15 line acting on both nicotinic and muscarinic acetylcholine receptors.
16 responses that result from poorly clustered acetylcholine receptors.
17 uld be attributed to inhibition of nicotinic acetylcholine receptors.
18 y activation of beta(2)-containing nicotinic acetylcholine receptors.
19 ncing myelination by deleting the muscarinic acetylcholine receptor 1 in oligodendrocyte precursor ce
20 gand-gated ion channel the Torpedo nicotinic acetylcholine receptor(10,11), the large body of structu
21 hat the Chrm4 transcript encoding muscarinic acetylcholine receptor 4 (M4) is excessively translated,
22 We and others have investigated muscarinic acetylcholine receptor 4 (M4) positive allosteric modula
24 target postsynaptic proteins, primarily the acetylcholine receptor (AChR) and inhibit signaling at t
25 at the neuromuscular junction, primarily the acetylcholine receptor (AChR) and the muscle-specific ki
26 cle mutation caused progressive denervation, acetylcholine receptor (AChR) cluster fragmentation, and
27 protein at synapse), which is essential for acetylcholine receptor (AChR) clustering and NMJ (neurom
28 the level of rapsyn, a protein necessary for acetylcholine receptor (AChR) clustering; and expression
31 associated with transformation of the muscle acetylcholine receptor (AChR) into an inhibitory channel
32 The maintenance of a high density of the acetylcholine receptor (AChR) is the hallmark of the neu
33 xamined expression of genes involved in anti-acetylcholine receptor (AChR) response in MG, MHC class
34 rs, many involving the muscle-type nicotinic acetylcholine receptor (AChR), although there are aspect
35 une disease caused by antibodies against the acetylcholine receptor (AChR), muscle-specific kinase (M
36 he outer leaflet of the plasma membrane, and acetylcholine receptor (AChR), which is a well-character
37 tin, a two-pass transmembrane protein, as an acetylcholine receptor (AChR)-associated protein, and we
38 er they produce autoantibodies targeting the acetylcholine receptor (AChR-MG) or muscle specific kina
40 ween motoneurons and skeletal muscles, where acetylcholine receptors (AChRs) are concentrated to cont
41 d protein, is required for the clustering of acetylcholine receptors (AChRs) at synaptic sites betwee
43 ing the timing of expression of postsynaptic acetylcholine receptors (AChRs) impacts presynaptic rele
44 for the proper distribution of extrasynaptic acetylcholine receptors (AChRs) in Caenorhabditis elegan
45 BLA principal neurons through activation of acetylcholine receptors (AChRs), (2) enhances glutamater
46 umulation of the neurotransmitter receptors, acetylcholine receptors (AChRs), to the postsynaptic mem
53 ipts of several targets, including nicotinic acetylcholine receptor alpha 1 and alpha 2 subunit, the
60 a hypothesized role for the alpha7-nicotinic acetylcholine receptor (alpha7-nAChR) in the pathophysio
61 ormal and cancer cells, the alpha7 nicotinic acetylcholine receptor (alpha7-nAChR), was more highly e
62 ypothesized that agonism on alpha7 nicotinic acetylcholine receptor (alpha7nAChR) in fetal microglia
63 ed chronic inflammation via alpha7 nicotinic acetylcholine receptor (alpha7nAChR) signaling. However,
64 show that ILC2s express the alpha7-nicotinic acetylcholine receptor (alpha7nAChR), which is thought t
65 linergic fibers through the alpha7-nicotinic acetylcholine receptor (alpha7nAChR), whose activation d
66 tor of the antiinflammatory alpha7 nicotinic acetylcholine receptor (alpha7nAChR/CHRNA7) that is also
68 ation of neural signals and alpha7 nicotinic acetylcholine receptors (alpha7nAChRs) on splenic macrop
69 s, RV inflammation, and RV alpha-7 nicotinic acetylcholine receptor and muscarinic acetylcholine type
71 ers displayed increased distinct clusters of acetylcholine receptors and axon terminals exhibited num
73 the epithalamus, densely expresses nicotinic acetylcholine receptors and is critical for nicotine int
75 Expression of nicotinic (alpha-7 nicotinic acetylcholine receptor) and muscarinic (muscarinic acety
76 n oligodendrocyte glycoprotein, aquaporin 4, acetylcholine receptor, and muscle-specific kinase) was
77 site is the alpha6 subunit of the nicotinic acetylcholine receptors, and different mutations in this
78 hroidine (DHbetaE), the most potent nicotine acetylcholine receptor antagonist (nAChR) of the Erythri
80 that scopolamine, a nonselective muscarinic acetylcholine receptor antagonist, produces rapid antide
81 ropilin-1 antibodies as well as by nicotinic acetylcholine receptor antagonists, suggesting that thes
82 -up was unremarkable except for detection of acetylcholine receptor antibodies in the serum (21.30 nm
83 of 24 OMG patients who were seropositive for acetylcholine receptor antibody (AchR Ab) converted to G
84 a gravis of less than 5 years' duration, had acetylcholine receptor antibody titres of 1.00 nmol/L or
85 eaningful improvements in patients with anti-acetylcholine receptor antibody-positive refractory gene
94 defects, including increased synaptic area, acetylcholine receptor area and density, and extent of p
96 cur within seconds of blocking or unblocking acetylcholine receptors at the mouse neuromuscular junct
97 of response to rituximab in the treatment of acetylcholine receptor autoantibody-positive (AChR+) gen
98 iR-1010 or its binding site in the nicotinic acetylcholine receptor beta2 (nAcRbeta2) 3'UTR fail to g
99 ibrations in the presence and absence of the acetylcholine receptor blockers d-tubocurarine and alpha
100 e was due to autoimmunity against muscarinic acetylcholine receptors, blocking their activation.
101 steric modulators (PAMs) of alpha7 nicotinic acetylcholine receptor can increase channel activation b
103 gand-gated channels and how mutations in the acetylcholine receptor cause congenital myasthenic syndr
105 ination/retraction, vesicle accumulation and acetylcholine receptor clustering and acetylcholinestera
107 ing organ of vertebrate species, a nicotinic acetylcholine receptor composed only of alpha9 subunits
109 yramidal cells express specialized nicotinic acetylcholine receptors containing the alpha5 subunit en
110 This work suggests that overstimulation of acetylcholine receptors could disrupt neuronal processin
113 ergic agonists for a cohort of patients with acetylcholine receptor deficiency on anticholinesterase
115 d a disease model to mirror the treatment of acetylcholine receptor deficiency, and demonstrate impro
116 can be explained in an experimental model of acetylcholine receptor deficiency, the most common form
117 SS), or secondhand smoke, promoted nicotinic acetylcholine receptor-dependent exacerbation of AA and
119 Lypd6, an endogenous modulator of nicotinic acetylcholine receptors, enhances experience-dependent p
121 ntiinflammatory effects via alpha7 nicotinic acetylcholine receptor-expressing splenic macrophages.
122 sely arranged myosin heavy chain and reduced acetylcholine receptor expression per immunocytochemical
123 onsmokers following stimulation of nicotinic acetylcholine receptors (familywise error-corrected P <
124 myoblast differentiation and aggregation of acetylcholine receptors for the establishment of neuromu
125 bind to the binding pocket of the muscarinic acetylcholine receptor formed by transmembrane alpha-hel
127 rons receive cholinergic input via nicotinic acetylcholine receptors from the Kenyon cells; knocking
128 at most synaptic sites, induction of "fetal" acetylcholine receptor gamma subunit (AChRgamma), reduct
132 ors (PAMs) of the M(1) subtype of muscarinic acetylcholine receptor have emerged as an exciting new a
133 selective activators of the M(4) muscarinic acetylcholine receptor have potential as a novel treatme
136 out the physiological function of muscarinic acetylcholine receptors in learning in adult flies.
137 the developmental switch from fetal to adult acetylcholine receptors in muscle (AChRs) and the functi
138 This strongly suggests a role of muscarinic acetylcholine receptors in the generalized sensitization
139 predict alcohol, and suggest that nicotinic acetylcholine receptors in the NAc are critical for this
140 encodes the alpha3 subunit of the nicotinic acetylcholine receptor, in five affected individuals fro
141 h can also activate, potentiate, and inhibit acetylcholine receptors, including neuronal nicotinic re
142 nd nicotine in the two major brain nicotinic acetylcholine receptors interact differently with the py
143 rug scopolamine was used to block muscarinic acetylcholine receptors involved in working memory.
144 ies conducted on the extracellular domain of acetylcholine receptors, ion channels from prokaryote ho
147 vely apply our model to the human muscarinic acetylcholine receptor M1, finding four experimentally c
148 teric modulators (PAMs) of the M1 muscarinic acetylcholine receptor (M1 mAChR) are a promising strate
149 or to detect activation of the M1 muscarinic acetylcholine receptor (M1 mAChR) in vitro and in vivo M
150 ne receptors, particularly the M1 muscarinic acetylcholine receptor (M1 mAChR), which was previously
151 itulated with blockade of M1-type muscarinic acetylcholine receptors (M1-AChR); however, the cellular
152 with beta-arrestin binding to M1 muscarinic acetylcholine receptors (M1Rs) in two different binding
156 cini preferentially expressed the muscarinic acetylcholine receptor M3 and maintained physiological r
159 AuAbs to desmocollin 3 (Dsc3), M3 muscarinic acetylcholine receptor (M3AR), and secretory pathway Ca(
160 uction of antinuclear and anti-M3 muscarinic acetylcholine receptor (M3R) autoantibodies and impairme
161 teric modulators (PAMs) of the M1 muscarinic acetylcholine receptor (mAChR) achieve exquisite selecti
162 stibular afferents is mediated by muscarinic acetylcholine receptor (mAChR) activation and the subseq
165 ovel 1,4-dioxane analogues of the muscarinic acetylcholine receptor (mAChR) antagonist 2 was synthesi
167 e allosteric modulators of the M5 muscarinic acetylcholine receptor (mAChR) have been described, but
168 in signaling of the M1 subtype of muscarinic acetylcholine receptor (mAChR) in the prefrontal cortex
171 Selective activation of the M1 muscarinic acetylcholine receptor (mAChR) via a positive allosteric
172 We previously reported a form of muscarinic acetylcholine receptor (mAChR)-dependent long-term depre
173 tic studies further indicate that muscarinic acetylcholine receptor (mAchR)/Galphao signaling produce
175 ng in adult flies requires type A muscarinic acetylcholine receptors (mAChR-A), particularly in the g
176 mba snakes that primarily bind to muscarinic acetylcholine receptors (MAChRs) and modulate their func
178 racterized two types (A and B) of muscarinic acetylcholine receptors (mAChRs), which were expressed i
181 pecific mechanisms of alpha3beta4*-nicotinic acetylcholine receptor modulation by the prototoxin lynx
182 y labeled dibenzodiazepinone-type muscarinic acetylcholine receptor (MR) antagonists, including dimer
184 ve processes that are modulated by nicotinic acetylcholine receptor (nAChR) activation by cholinergic
185 ending plasma levels of the alpha7-nicotinic acetylcholine receptor (nAChR) agonist 3-(2,4-dimethoxyb
187 icotine or ABT-418, an alpha4beta2 nicotinic acetylcholine receptor (nAChR) agonist, normalized MSO t
188 GeXIVA inhibits the alpha9alpha10 nicotinic acetylcholine receptor (nAChR) and is analgesic in anima
189 These effects were blocked by the nicotinic acetylcholine receptor (nAChR) antagonist mecamylamine.
191 pha-conotoxin CIA, a potent muscle nicotinic acetylcholine receptor (nAChR) blocker with a significan
192 a desensitized state of the alpha7 nicotinic acetylcholine receptor (nAChR) have been associated with
193 with this soluble surrogate of the nicotinic acetylcholine receptor (nAChR) in a cooperative fashion,
197 ctivity of the muscle-type Torpedo nicotinic acetylcholine receptor (nAChR) is highly sensitive to li
199 rovide an improved model to assess nicotinic acetylcholine receptor (nAChR) ligands for treating chro
201 al role in the characterization of nicotinic acetylcholine receptor (nAChR) structure and function an
202 alpha7 (IC(50) 77.1 +/- 0.05 mum) nicotinic acetylcholine receptor (nAChR) subtypes, but the activit
203 interacting with alpha7-containing nicotinic acetylcholine receptor (nAChR) subtypes, leads to subnuc
204 e is known about the role of beta4 nicotinic acetylcholine receptor (nAChR) subunit encoded by this c
205 n CHRNA3, which encodes the alpha3 nicotinic acetylcholine receptor (nAChR) subunit gene, increases r
206 RNA3, the gene encoding the alpha3 nicotinic acetylcholine receptor (nAChR) subunit, increases vulner
207 for the alpha5, alpha3, and beta4 nicotinic acetylcholine receptor (nAChR) subunits, to nicotine add
208 A7, the gene coding for the alpha7 nicotinic acetylcholine receptor (nAChR), and manifest a variable
209 CHRNA7, encoding for the alpha7 nicotinic acetylcholine receptor (nAChR), has been suggested as a
214 ulation and synaptic clustering of nicotinic acetylcholine receptors (nAChR) during neurotrophic fact
215 vity of classical agonists for the nicotinic acetylcholine receptors (nAChR) has prompted us to ident
216 sociations between variants in the nicotinic acetylcholine receptors (nAChR) subunits and nicotine de
218 ed TGFBR2 and the nicotinic antiinflammatory acetylcholine receptor nAChRa7 as murine and human miR-2
219 ivation of 42 genes, including the nicotinic acetylcholine receptors nAChRalpha1 and nAChRalpha3, in
221 new group of inhibitors for muscle nicotinic acetylcholine receptors (nAChRs) and some neuronal nAChR
227 btx) and prevent its inhibition of nicotinic acetylcholine receptors (nAChRs) as a lead for the devel
230 Here, we show that activation of nicotinic acetylcholine receptors (nAChRs) by quantal release of a
232 ficant cholinergic innervation and nicotinic acetylcholine receptors (nAChRs) contribute greatly to t
233 t widely co-abused substances, and nicotinic acetylcholine receptors (nAChRs) contribute to the behav
234 hances nicotine-induced changes in nicotinic acetylcholine receptors (nAChRs) expressed on midbrain D
235 d shows high binding affinity with nicotinic acetylcholine receptors (nAChRs) expressed on the surfac
236 gically distinguishing alpha3beta2 nicotinic acetylcholine receptors (nAChRs) from closely related su
238 a suggest a complex interaction of nicotinic acetylcholine receptors (nAChRs) in regulating vestibula
241 nduced upregulation of alpha4beta2 nicotinic acetylcholine receptors (nAChRs) is associated with chan
247 but very little is known about how nicotinic acetylcholine receptors (nAChRs) regulate LHb activity.
248 ression and clustering of neuronal nicotinic acetylcholine receptors (nAChRs) remain poorly defined.
249 ping drugs that act at alpha4beta2 nicotinic acetylcholine receptors (nAChRs) to treat alcohol use di
250 t of aging on presynaptic neuronal nicotinic acetylcholine receptors (nAChRs) within the circuitry of
251 the highest density in alpha4beta2 nicotinic acetylcholine receptors (nAChRs) within the whole cortex
253 ear synapse involves alpha9alpha10 nicotinic acetylcholine receptors (nAChRs), which assemble in hair
260 We administered a novel alpha7 nicotinic acetylcholine receptor-negative allosteric modulator, BN
261 se results represent the first evidence that acetylcholine receptors negatively modulate muscle spind
263 dependence and stimulation of the nicotinic acetylcholine receptor on the ability to interpret valen
264 nd acute effects of stimulation of nicotinic acetylcholine receptors on behavioral and neural signatu
265 binding follows hyperbolic (M(4) muscarinic acetylcholine receptors) or nonhyperbolic relationships
266 cally prevented by the alpha4beta2 nicotinic acetylcholine receptor partial agonist and alpha7 recept
267 strategy is to selectively target muscarinic acetylcholine receptors, particularly the M1 muscarinic
268 his to be the case with the alpha7 nicotinic acetylcholine receptor positive allosteric modulator (PA
269 racemic preparation, is an alpha7 nicotinic acetylcholine receptor positive allosteric modulator (PA
270 r in animals through inhibition of nicotinic acetylcholine receptors present in the central nervous s
272 on of the ER-resident chaperone of nicotinic acetylcholine receptors, RIC-3, leads to increased muscl
273 f geniculocortical inputs with M2 muscarinic acetylcholine receptor-rich patches in layer 1 (L1) sugg
276 treatment reduced disease severity, lowered acetylcholine receptor-specific Abs, and decreased CD19(
278 igra pars reticulata (SNr) act on muscarinic acetylcholine receptor subtype 4 (M4) to oppose cAMP-dep
279 ith targeted disruption of single muscarinic acetylcholine receptor subtype genes (M(1) to M(5)) and
283 anges in alpha4, alpha3, and beta2 nicotinic acetylcholine receptor subunit mRNA levels in the nucleu
285 species from all five subtypes of muscarinic acetylcholine receptors, suggesting allosteric binding.
286 h ion channels of the ligand-gated nicotinic acetylcholine receptor superfamily (namely alpha-amino-3
287 tor ligand to activate a modified muscarinic acetylcholine receptor that is insensitive to acetylchol
288 ract may primarily target muscarinic subtype acetylcholine receptors that regulate memory processes.
289 losteric modulator (PAM) of alpha7 nicotinic acetylcholine receptors that, like 4BP-TQS and its activ
290 ryoEM structure of sAB bound human nicotinic acetylcholine receptor, this work demonstrates that thes
291 We assessed the contribution of muscarinic acetylcholine receptors to motivated behaviour in mice,
292 econdary Gi/o coupling, using the muscarinic acetylcholine receptor type 2 (M2R) as the primary Gi/o-
293 by CRF results in the activation muscarinic acetylcholine receptors type 5, which mediate potentiati
295 -inflammatory alpha7-nAChR (alpha7-nicotinic acetylcholine receptor) was similar in young SHR and WKY
297 vitro demonstrated that the mutant nicotinic acetylcholine receptors were unable to generate current
298 probe the ion channel pore of the nicotinic acetylcholine receptor, which is a prototypical Cys-loop
299 with nonselective antagonists of muscarinic acetylcholine receptors, which have many undesirable sid
300 ll types expressing alpha8 subunit nicotinic acetylcholine receptor, while SPO and cOv are characteri