ライフサイエンスコーパス: AChE

1 AChE catalyses the cleavage of acetylthiocholine chlorid

2 AChE in red blood cells is a surrogate for AChE in the n

3 AChE is clustered by the collagen Q in the synaptic clef

4 AChE was immobilized on the gold surface of an SPR senso

5 AChE was solubilized from frozen RBC by addition of 1% T

6 AChE+ cells were first detectable in an embryonic day (E

7 positions 4, 6, or 7 conferred both acetyl (AChE) and butyryl (BuChE) cholinesterase inhibitory acti

8 Acetylcholinesterase (AChE) biosensor was developed through silica sol-gel (Si

9 Acetylcholinesterase (AChE) converts ACh to choline, which in turn is oxidized

10 Acetylcholinesterase (AChE) inhibitors are commonly used pesticides that can e

11 Acetylcholinesterase (AChE) inhibitors are potentially lethal but also have ap

12 Acetylcholinesterase (AChE) is crucial for degrading acetylcholine at choliner

13 Acetylcholinesterase (AChE) is highly expressed at sites of nerve-muscle conta

14 enediamine) (PoPD) and acetylcholinesterase (AChE) and choline oxidase (ChO) enzymes were fabricated

15 transferase (ChAT) and acetylcholinesterase (AChE) are the decisive enzymatic activities regulating t

16 tion of human BChE and acetylcholinesterase (AChE) with metaproterenol, isoproterenol, and newly synt

17 ously established AOP, acetylcholinesterase (AChE) inhibition.

18 and their potential as acetylcholinesterase (AChE) and butyrylcholinesterase (BuChE) inhibitors was a

19 ibitory effect on both acetylcholinesterase (AChE) and butyrylcholinesterase (BuChE).

20 The cholinesterases, acetylcholinesterase (AChE) and butyrylcholinesterase, are primary targets of

21 tochrome oxidase (CO), acetylcholinesterase (AChE), and vesicular glutamate transporter-2 (VGluT2) pr

22 nitin, a novel dimeric acetylcholinesterase (AChE) inhibitor derived from tacrine, prevented Abeta ol

23 's disease (AD), i.e., acetylcholinesterase (AChE) and monoamine oxidase B (MAO B), a series of multi

24 sitive electrochemical acetylcholinesterase (AChE) biosensor was successfully developed on polyanilin

25 genetically-engineered acetylcholinesterase (AChE) immobilized in a azide-unit water-pendant polyviny

26 ons between the enzyme acetylcholinesterase (AChE) and two compound classes consisting of N-[2-(dieth

27 target was the enzyme acetylcholinesterase (AChE), and the AChE-ICERs produced were used in a liquid

28 ive site of the enzyme acetylcholinesterase (AChE).

29 linking of the enzymes acetylcholinesterase (AChE) and choline oxidase (ChO).

30 immobilizing enzymes, acetylcholinesterase (AChE) and choline oxidase (ChO), on the surface of iron

31 ds displayed excellent acetylcholinesterase (AChE) inhibitory potencies and interesting capabilities

32 c compounds, exhibited acetylcholinesterase (AChE) inhibitory activity and also displayed effective i

33 ioned, and stained for acetylcholinesterase (AChE) to identify the NMJs.

34 ins were performed for acetylcholinesterase (AChE), nicotinamide adenine dinucleotide phosphate-diaph

35 Human acetylcholinesterase (AChE) is a significant target for therapeutic drugs.

36 ies, and inhibit human acetylcholinesterase (AChE).

37 tes for OP-inactivated acetylcholinesterase (AChE) were lower compared to 2-PAM but greater compared

38 rgic factors including acetylcholinesterase (AChE), choline acetyltransferase (ChAT), choline transpo

39 ecticides that inhibit acetylcholinesterase (AChE) enzyme activity in the salmon nervous system, ther

40 arfare agent inhibited acetylcholinesterase (AChE) with promising in vitro potential was developed by

41 d methylcarbamate (MC) acetylcholinesterase (AChE) inhibitors.

42 s genetically modified acetylcholinesterase (AChE) enzymes B394, B4 and wild type B131.

43 tate receptor (NMDAR), acetylcholinesterase (AChE), and monoamine oxidase B (MAO-B).

44 stinct localization of acetylcholinesterase (AChE) and butyrylcholinesterase (BChE) at the NMJ to bri

45 ated via inhibition of acetylcholinesterase (AChE) and butyrylcholinesterase (BChE), and tyrosinase (

46 valently, a mixture of acetylcholinesterase (AChE) and choline oxidase (ChO) onto nanocomposite of ch

47 sensitive detection of acetylcholinesterase (AChE) and its inhibitor using a cationic surfactant-deco

48 ated the expression of acetylcholinesterase (AChE) and the density of myelinated axons throughout pos

49 catalytic subunits of acetylcholinesterase (AChE) are anchored in the basal lamina of the neuromuscu

50 eries of inhibitors of acetylcholinesterase (AChE) have been screened by back-scattering interferomet

51 crystal structures of acetylcholinesterase (AChE) in complex with galantamine derivatives.

52 versible inhibition of acetylcholinesterase (AChE) in the nervous system.

53 ial period and that of acetylcholinesterase (AChE) increased during a later time period.

54 ns through blockade of acetylcholinesterase (AChE) whereas antidepressant-like effects can be produce

55 ced by the addition of acetylcholinesterase (AChE), and thus appears to involve ACh spillover.

56 d in the regulation of acetylcholinesterase (AChE), which is a key protein of the cholinergic system

57 ve to perturbations of acetylcholinesterase (AChE), while slow non-alpha7 receptor-mediated EPSCs are

58 sprouting response of acetylcholinesterase (AChE)-positive fibers, a phenotype reminiscent of human

59 nd peripheral sites of acetylcholinesterase (AChE).

60 versible inhibition of acetylcholinesterase (AChE).

61 igand binding sites on acetylcholinesterase (AChE) comprise an active center, at the base of a deep a

62 nic anhydrase (BCA) or acetylcholinesterase (AChE) and inhibit their catalytic activities.

63 ntidotes to reactivate acetylcholinesterase (AChE) inhibited by organophosphorus nerve agents.

64 ther biological roles, acetylcholinesterase (AChE, EC 3.1.1.7), encoded by two ace in most insects, c

65 is, a highly sensitive acetylcholinesterase (AChE) cyclic voltammetric biosensor based on zinc oxide

66 s also a submicromolar acetylcholinesterase (AChE) inhibitor and therefore, could contribute, through

67 y of newly synthesized acetylcholinesterase (AChE) molecules do not assemble into catalytically activ

68 entral nervous system, acetylcholinesterase (AChE) is present in a tetrameric form that is anchored t

69 w that miR-608 targets acetylcholinesterase (AChE) and demonstrate weakened miR-608 interaction with

70 RNA) homologous to the acetylcholinesterase (AChE) and ecdysone receptor (EcR) genes of B. tabaci, re

71 alysis (EDA) using the acetylcholinesterase (AChE) bioassay and metabolomics.

72 the performance of the acetylcholinesterase (AChE) enzyme.

73 ke its homologs in the acetylcholinesterase (AChE) family, ChEL possesses two carboxyl-terminal alpha

74 By utilizing the acetylcholinesterase (AChE) mediated hydrolysis of acetylthiocholine to thioch

75 and a high throughput acetylcholinesterase (AChE) assay was developed.

76 tory properties toward acetylcholinesterase (AChE) in relation to tacrine.

77 the conjugates toward acetylcholinesterase (AChE), butyrylcholinesterase (BChE) and structurally clo

78 ry described here uses acetylcholinesterase (AChE) and produces an unambiguous color change when the

79 binding mechanism with acetylcholinesterase (AChE) as its more potent counterparts such as sarin and

80 lves reacting ACh with acetylcholinesterase (AChE) to form choline that is in turn oxidized by cholin

81 nd surface coated with acetylcholinesterase (AChE) were attached to gold screen printed electrodes to

82 in and conjugated with acetylcholinesterase (AChE), an enzyme specific for acetylcholine, resulting i

83 reviously that insect acetylcholinesterases (AChEs) could be selectively and irreversibly inhibited b

84 A gamma-secretase inhibitor did not affect AChE transcript levels or enzyme activity in SN56 (APP69

85 ped a computational strategy and designed an AChE variant bearing 51 mutations that improved core pac

86 tively, using C-dots@RGO (0.4 mg.mL(-1)) and AChE and ChOx at the activities of 0.5 and 0.1 unit.mL(-

87 contrast, addition of CB[7] to AChE*4(4) and AChE*5(4) results in the formation of thermodynamically

88 ble ternary complexes AChE*4(4)*CB[7](4) and AChE*5(4)*CB[7](4) that are catalytically inactive.

89 ermined at various concentrations of ACh and AChE.

90 vivo interactions of the nAChR agonists and AChE inhibitors.

91 Targeted chemical analysis and AChE bioassay were performed on the cartridge extracts.

92 " Applying immunohistochemistry for ChAT and AChE on sections of the chicken retina, we here have rev

93 nthesis established SAR delineating ChK1 and AChE activities and allowing identification of new leads

94 rofiles of the binding between compounds and AChE revealed class-dependent differences of the entropy

95 is Water Maze Test, Radial Arm Maze Test and AChE activity in scopolamine induced amnetic rats.

96 As AChE is deeply conserved, widely expressed outside of th

97 and in turn increases total cell-associated AChE activity and active tetramer secretion.

98 showed good inhibitory activities at MAO-B, AChE, and BChE but low selectivity.

99 When both AChE and BChE were inhibited, the spillover increased an

100 small transmembrane protein anchor of brain AChE.

101 but now also correlating with in vivo brain AChE inhibition, indicating that ACh is the ultimate OP-

102 e (Ch) which in turn interacts with AuQC@BSA-AChE and quenches its fluorescence, enabling sensing.

103 Further, the sensor, AuQC@BSA-AChE can be easily coated on paper and an efficient and

104 This suggests that AuQC@BSA-AChE has an excellent potential to be used for diagnosis

105 The fluorescent intensity of AuQC@BSA-AChE is sensitive towards acetylcholine in range of 10nM

106 fic for acetylcholine, resulting in AuQC@BSA-AChE.

107 of how retinal networks became dominated by AChE or by ChAT reactivities.

108 ing the beta-amyloid aggregation promoted by AChE.

109 eased tolerance to the insecticide carbaryl (AChE-inhibitor) can induce increased tolerance to other

110 purification method to enrich red blood cell AChE (RBC AChE) as a biomarker of exposure.

111 , indicating the future IPL, pairs of ChAT+ /AChE- /Brn3a- cells appeared between E7/8.

112 AOs) and acetyl- and butyryl-cholinesterase (AChE and BChE) inhibitors.

113 f thermodynamically stable ternary complexes AChE*4(4)*CB[7](4) and AChE*5(4)*CB[7](4) that are catal

114 In conclusion, AChE is regulated in two neuronal cell lines by APP in a

115 states for reactivation of the OP-conjugated AChE.

116 ited nAChR in vivo without the corresponding AChE inhibition, possibly via a reactive ketene metaboli

117 Despite precursor binding to crystalline AChE, coupling of rapid electric field fluctuations in t

118 on, whereas overexpression of PUM2 decreased AChE activity.

119 Denatured AChE was eluted with 1% trifluoroacetic acid.

120 Mutations in COLQ cause endplate AChE deficiency.

121 xon 16 identified in a patient with endplate AChE deficiency causes exclusive skipping of exon 16.

122 The peptides act to enhance AChE folding thereby rescuing them from reticulum degrad

123 The enzyme, AChE hydrolyzes acetylcholine (ACh) to choline (Ch) whic

124 Erythrocyte AChE activity was measured using the EQM Test-mate syste

125 potent inhibitor of acetylcholine esterase (AChE) and unsuitable for development.

126 ng the Ellman assay to measure ACh esterase (AChE) activity that breaks down ACh, the second experime

127 llow the activity of acetylcholine esterase, AChE, and to probe its inhibition.

128 that muscle cells, or cell lines expressing AChE catalytic subunits, incubated with synthetic prolin

129 On either side of a faint AChE+ band, indicating the future IPL, pairs of ChAT+ /A

130 At pH 7.4, the final assembly, Naf-FCNTs/AChE-ChO((10:1))/PoPD/CF(Elip), was observed to have hig

131 Their dual site binding for AChE, supported by kinetic and molecular modeling studie

132 a cumulative 0.05 of the predicted EC50 for AChE inhibition, as determined from single chemical conc

133 tivity (IC50 value of 0.30 +/- 0.01 muM) for AChE and (1.84 +/- 0.03 muM) for BuChE.

134 scontinuous layer 2 modules are positive for AChE, NADPH-d, GAD, and CO throughout the rostrocaudal L

135 bservations point to a prime requirement for AChE to interconvert dynamically between sequential conf

136 AChE in red blood cells is a surrogate for AChE in the nervous system.

137 In animals lacking functional AChE in the CNS (PRiMA(-/-) mice) the EPSCs resembled th

138 dotes that promote the release of functional AChE by an unknown reactivation mechanism.

139 de chain motions in the gorge that may guide AChE toward a transient state favoring syn-triazole form

140 Here, we characterize 10 human (h) AChE mutants that, when coupled with an oxime, give rise

141 t human acetyl- and butyrylcholinesterase (h-AChE and h-BuChE), being more potent than the parent inh

142 The tacrine-silibinin codrug shows high AChE and BChE inhibition, neuroprotective effects, lacks

143 d molecular genetic decreases in hippocampal AChE activity increased anxiety- and depression-like beh

144 that shRNA-mediated knockdown of hippocampal AChE represents a model for anxiety- and depression-like

145 With the most efficient human AChE mutant Y337A/F338A, we show enhanced reactivation r

146 Thirty chemicals found to inhibit human AChE in the ToxCast assay were examined with respect to

147 -, tabun- and ethyl paraoxon-inhibited human AChE.

148 nd to be the most potent inhibitors of human AChE (hAChE), demonstrating IC50 values of 0.0154 and 0.

149 as mixed-type reversible inhibitors of human AChE and BuChE with high active site contact.

150 nhibition of the catalytic activity of human AChE and, more importantly, in the in vitro neutralizati

151 These crystals of human AChE provide a more accurate platform for further drug d

152 high resolution crystal structures of human AChE, alone and in complexes with drug ligands; donepezi

153 3,604-458,597 M(-1)sec(-1) but spared human AChE.

154 ifferential HTS analysis including the human AChE, several structurally diverse, potent, and selectiv

155 r's disease drug, binds differently to human AChE than it does to Torpedo AChE.

156 on irreversibly inhibited mosquito and human AChEs with k(inact)/K(I) values of 1,915 and 1,507 M(-1)

157 method was successfully applied to identify AChE inhibitors in a wastewater treatment plant (WWTP) e

158 m hydrolysis of acetylcholine by immobilized AChE.

159 ate long-lasting stress-inducible changes in AChE's promoter choices, identify the chromatin changes

160 A 1-U/mL decrease in AChE activity was associated with a 2.86-mmHg decrease i

161 P resulted in a significant up-regulation in AChE mRNA levels.

162 le or greater reactivation of OP-inactivated AChE and OP-inactivated BChE.

163 Administration of fluoxetine also increased AChE activity throughout the brain, with the greatest ch

164 The remaining 22 compounds may inhibit AChE in vivo either directly or as a result of metabolic

165 E into reactivators of nerve agent-inhibited AChE.

166 ncy for reactivation of Sarin (GB)-inhibited AChE and BChE.

167 inhibitors, as they progressively inhibited AChE 960 to 80 times more slowly than BChE(UU).

168 presin can be used to enrich soman-inhibited AChE solubilized from 8 mL of frozen human erythrocytes,

169 d to pharmacomodulate RS67333 to enhance its AChE inhibitory activity to take advantage of this pleio

170 Pulse-chase studies of isotopically labeled AChE molecules show that the enzyme is rescued from intr

171 n vivo completely abolished the long-lasting AChE-related and behavioral stress effects.

172 These features launched AChE as a reaction vessel for in situ click-chemistry sy

173 on, subband "a" presented more ChAT but less AChE; in subband "d" this pattern was reversed.

174 nd demonstrate the early onset of adult-like AChE expression in primary auditory cortex in O. garnett

175 Type-I cells had increased ChAT and lost AChE; type-II cells presented less ChAT, but some AChE o

176 This method can be used to screen for mixed AChE inhibitors, agents that have shown high efficacy ag

177 confirm that reliable fluorescent monitoring AChE-catalyzed hydrolysis of ACh is possible through the

178 ChEL) allows for dimerization with monomeric AChE, proving exposure of the carboxyl-terminal helices

179 eversibly inhibited African malaria mosquito AChE with bimolecular inhibition rate constants (k(inact

180 ect neighbors of SACs tended to express much AChE.

181 t antidote HI-6 in complex with Mus musculus AChE covalently inhibited by the nerve agent sarin.

182 nteracted enzyme-armored MWCNT-OPH and MWCNT-AChE along with a set of cushioning bilayers consisting

183 , suggesting an adaptation to the absence of AChE.

184 n of BChE counteracts the positive action of AChE inhibition.

185 Notably, the classical esterase activity of AChE is dispensable for this activity.

186 choline to thiocholine where the activity of AChE is inhibited by the presence of organophosphate pes

187 led the probing of the enzymatic activity of AChE through the hemin/G-quadruplex-catalyzed aerobic ox

188 Subsequent crystallographic analyses of AChE complexes with the TZ2PA6 regioisomers demonstrated

189 Analysis of AChE expression indicated that, in contrast to evidence

190 were observed of the proline-rich anchor of AChE, PRiMA, no changes were seen in mRNA levels of the

191 iculum network where they induce assembly of AChE tetramers.

192 A strong association of AChE with PRiMA at the plasma membrane is therefore a fe

193 ARs in terms of their inhibition capacity of AChE.

194 in the brain express high concentrations of AChE enzymic activity at their neuronal membranes.

195 the large scale intracellular degradation of AChE previously observed and indicate that simple peptid

196 ing high promise for label-free detection of AChE and its inhibitors.

197 n this article, we describe the detection of AChE inhibitor binding by SPR without the use of competi

198 dent samples, the adult-like distribution of AChE in the core area of auditory cortex, dense bands in

199 on of the pathological chaperoning effect of AChE toward the aggregation of both the beta-amyloid pep

200 ough silica sol-gel (SiSG) immobilisation of AChE on the carbon paste electrode (CPE) and used as wor

201 The pharmacological inactivation of AChE by neostigmine caused the appearance of an ultra-sl

202 -range spillover produced by inactivation of AChE.

203 function than the simultaneous inhibition of AChE and BChE because the concomitant inhibition of BChE

204 Compound 44 showed mixed inhibition of AChE in the enzyme kinetic studies.

205 In myasthenic rats, selective inhibition of AChE is more effective in rescuing muscle function than

206 nds exhibited moderate to high inhibition of AChE-induced Abeta1-42 aggregation and noticeable in vit

207 molecules were then tested as inhibitors of AChE and as binders of the N-methyl-d-aspartate (NMDA) r

208 e new compounds were nanomolar inhibitors of AChE and showed micromolar affinities for NMDAR.

209 utilized to develop reversible inhibitors of AChE into reactivators of nerve agent-inhibited AChE.

210 l changes due to shRNA-mediated knockdown of AChE were rescued by coinfusion of an shRNA-resistant AC

211 of the brain known to express high levels of AChE enzymic activity including cranial nerve motor neur

212 nd SH-SY5Y substantially decreased levels of AChE mRNA, protein, and catalytic activity.

213 In silico docking using a model of AChE permitted rationalization of the observed SAR.

214 levels as low as 100 pM (22,000 molecules of AChE) can be detected.

215 ors and the peripheral anionic site (PAS) of AChE.

216 Y (APP695) cells, showing that regulation of AChE by APP does not require the generation of AICD or a

217 t the observed transcriptional repression of AChE is mediated by the E1 region of APP, specifically i

218 sion from 18 to 24 months led to reversal of AChE sprouting, resolution of Gallyas-positive and Alz50

219 ropidium from the peripheral anionic site of AChE, preventing the beta-amyloid aggregation promoted b

220 e site as well as peripheral anionic site of AChE.

221 -soaking procedures and solved structures of AChE complexes with the TZ2PA5 regioisomers and their TZ

222 ffinity about five times higher than that of AChE.

223 lysis rates were compared in solution and on AChE conjugates and analyzed in terms of the ionization

224 The proposed biosensor based on AChE immobilized in sol-gel matrix was used for the dete

225 echanism of intrinsic reactivation of the OP-AChE conjugate and penetration of the blood-brain barrie

226 enhanced intrinsic reactivity against the OP-AChE target combined with favorable pharmacokinetic prop

227 d UV-vis methods on the MWCNT-(PEI/DNA)2/OPH/AChE biosensor, showing great potential in large screeni

228 e (BuCh) as an internal standard, the HRP-Os/AChE-ChO and PB/AChE-ChO electrodes exhibited excellent

229 enhanced detection capability of the HRP-Os/AChE-ChO and PB/AChE-ChO electrodes in combination with

230 oM or 38 amol were determined for the HRP-Os/AChE-ChO electrode.

231 Using an EDA approach, other AChE inhibiting candidates were identified in the neutra

232 elective inhibitory action against BChE over AChE and CaE.

233 The GC/MWCNT/PANI/AChE biosensor exhibited detection limits of 1.4 and 0.9

234 nternal standard, the HRP-Os/AChE-ChO and PB/AChE-ChO electrodes exhibited excellent linear responses

235 ion capability of the HRP-Os/AChE-ChO and PB/AChE-ChO electrodes in combination with efficient CE sep

236 limit of detection for ACh and Ch at the PB/AChE-ChO electrode was 5 microM or 9.5 fmol.

237 rid, and pirimicarb, and was the most potent AChE inhibitor.

238 The most potent AChE inhibitors were 120 (3-(2-aminoethyl) indolin-4-yl

239 s with a PUM2 specific antibody precipitated AChE mRNA, suggesting that PUM2 binds to the AChE transc

240 mote AChE tetramerization in cells producing AChE.

241 omain of collagen Q is sufficient to promote AChE tetramerization in cells producing AChE.

242 on method to enrich red blood cell AChE (RBC AChE) as a biomarker of exposure.

243 esent work was to provide an alternative RBC AChE enrichment strategy, by binding RBC AChE to Hupresi

244 RBC AChE enrichment strategy, by binding RBC AChE to Hupresin affinity gel.

245 The same protocol was used for 20 mL of RBC AChE inhibited with a soman model compound.

246 The red, but not viscous, RBC AChE solution was loaded on a Hupresin affinity column.

247 tinguish between active and OP-inhibited RBC-AChE are discussed.

248 nds showed a promising ability to reactivate AChE inhibited by various types of CWA in vitro.

249 owed HFD consumption to significantly reduce AChE activity in the frontal cortex, hypothalamus and mi

250 in vitro potency with significantly reduced AChE activity.

251 say method was validated using the reference AChE inhibitors tacrine and galanthamine.

252 s with shRNAs specific for PUM2 up-regulated AChE expression, whereas overexpression of PUM2 decrease

253 e that PUM2 binds to AChE mRNA and regulates AChE expression translationally at the neuromuscular syn

254 rescued by coinfusion of an shRNA-resistant AChE transgene into the hippocampus and reversed by syst

255 re washed off with 3 M NaCl, while retaining AChE bound to Hupresin.

256 ened miR-608 interaction with the rs17228616 AChE allele having a single-nucleotide polymorphism (SNP

257 Mean (+/- SD) AChE activity was 3.14 +/- 0.49 U/mL.

258 ygote for the minor rs17228616 allele showed AChE elevation and CDC42/IL6 decreases compared with maj

259 ion to its role in nervous system signaling, AChE can also modulate non-neuronal cell properties, alt

260 type-II cells presented less ChAT, but some AChE on their surfaces.

261 port our hypothesis that the insect-specific AChE cysteine is a unique and unexplored target to devel

262 We find that a Tg-AChE chimera (swapping AChE in place of ChEL) allows for dimerization with mono

263 interact as mixtures to produce synergistic AChE inhibition at concentrations near or above the uppe

264 nts expressing dsRNA homologous to B. tabaci AChE and EcR were constructed by fusing sequences derive

265 igmine or virally delivered shRNAs targeting AChE into the hippocampus.

266 We find that a Tg-AChE chimera (swapping AChE in place of ChEL) allows for

267 ight be attributed to a mechanism other than AChE inhibition.

268 ense morpholino or CRISPR-Cas9) confirm that AChE is specifically required in the gut endoderm tissue

269 Moreover, we find that AChE and soluble neuroligins also can bind to the upstre

270 in this capacity in vivo Here, we show that AChE plays an essential non-classical role in vertebrate

271 We have previously shown that AChE in skeletal muscle is regulated in part post-transl

272 The AChE activities were decreased to 32% to 85% of control

273 The AChE-catalyzed hydrolysis of acetylthiocholine to the th

274 To test this hypothesis, we administered the AChE inhibitor physostigmine to mice and demonstrated an

275 enzyme acetylcholinesterase (AChE), and the AChE-ICERs produced were used in a liquid chromatograph-

276 Specifically, the AChE gene encoding the acetylcholine-hydrolyzing enzyme

277 Noteworthy is that the AChE LC sensor shows a very high sensitivity for the det

278 AChE mRNA, suggesting that PUM2 binds to the AChE transcripts in a complex.

279 When the sensor with the AChE enzyme is put in contact with acetylthiocholine (AT

280 und inhibits this signal by binding with the AChE enzyme.

281 nsional retention alignment as well as their AChE inhibition activity.

282 ity (>0.9) separation was achieved and three AChE inhibitors (tiapride, amisulpride, and lamotrigine)

283 In contrast, addition of CB[7] to AChE*4(4) and AChE*5(4) results in the formation of ther

284 We conclude that PUM2 binds to AChE mRNA and regulates AChE expression translationally

285 different order of effectiveness compared to AChE inhibition.

286 Exposure of Xenopus embryos to AChE-inhibiting chemicals results in severe defects in i

287 d EPSCs are reliable and highly sensitive to AChE activity.

288 rently to human AChE than it does to Torpedo AChE.

289 main showed specific binding using wild type AChE 3'-UTR RNA segment that was abrogated by mutation o

290 Typical AChE-based interfering species did not affect the PHA pe

291 In contrast, tacrine and donepezil, typical AChE inhibitors, could not prevent synaptic impairments

292 he optical appearance was then observed when AChE was transferred onto the Myr-decorated LC interface

293 ocalized at the neuromuscular junction where AChE mRNA concentrates.

294 s, although it remains controversial whether AChE functions in this capacity in vivo Here, we show th

295 is of one of those compounds in complex with AChE allowed rationalizing the outstanding activity data

296 these neurones, PRiMA also co-localizes with AChE immunoreactivity at the plasma membrane.

297 ic blood pressure (DBP), and heart rate with AChE activity, living with flower workers, duration of c

298 Under optimum conditions, the Pt/ZnO/AChE/Chitosan bio-electrode detected carbosulfan ranging

299 The developed Pt/ZnO/AChE/Chitosan bio-electrode showed good recovery (99.06-

300 The Pt/ZnO/AChE/Chitosan bio-electrode was employed for the electro