ライフサイエンスコーパス: cholinesterase

1 e protein RIC-3 (resistance to inhibitors of cholinesterase).

2 its through mechanisms other than inhibiting cholinesterase.

3 n endoplasmic reticulum retention of the two cholinesterases.

4 neurotransmission through inhibition of the cholinesterases.

5 bind covalently to the active-site serine of cholinesterases.

6 role in determining substrate specificity in cholinesterases.

7 hree or four major oligosaccharides in other cholinesterases.

8 ornica acetylcholinesterase, and recombinant cholinesterases.

9 esized and purified PIP exhibited binding to cholinesterases.

10 they can suppress hyperglycemia and inhibit cholinesterases.

11 ing for the complete amino acid sequences of cholinesterase 1 (ChE1) and cholinesterase 2 (ChE2) from

12 in) compared with tetrameric forms of plasma cholinesterases (1902-3206 min).

13 cid sequences of cholinesterase 1 (ChE1) and cholinesterase 2 (ChE2) from amphioxus.

14 have shown that resistance to inhibitors of cholinesterase 8 (Ric-8) proteins regulate an early step

15 model organisms, resistance to inhibitors of cholinesterase 8 (Ric-8), a G protein alpha (G alpha) su

16 e have identified resistant to inhibitors of cholinesterase 8 (Ric8) as a nonreceptor guanine nucleot

17 ric-8 (resistance to inhibitors of cholinesterase 8) genes have positive roles in variegate

18 Resistance to inhibitors of cholinesterase 8A (Ric-8A) is a highly evolutionarily co

19 nist and Ric-8A (resistance to inhibitors of cholinesterase-8A).

20 Resistance to Inhibitors of Cholinesterase A (Ric-8A) is a 60-kDa cytosolic protein

21 ls in bedding, hepatitis A antibodies, serum cholinesterase (a marker of organophosphorus exposure),

22 The cholinesterases, acetylcholinesterase (AChE) and butyryl

23 mine oxidases (MAOs) and acetyl- and butyryl-cholinesterase (AChE and BChE) inhibitors.

24 However, previous reports describe cholinesterase activities in several plant species and w

25 Blood cholinesterase activity and insecticide concentration we

26 Thus, brain imaging of cholinesterase activity associated with Abeta plaques ha

27 Imaging cholinesterase activity associated with Abeta plaques in

28 The samples exhibited no in vitro anti-cholinesterase activity but presented strong antidiabeti

29 me can also be separated from the endogenous cholinesterase activity by its subcellular localization

30 However the presence of cholinesterase activity has been described also in non-m

31 several diseases, the antidiabetic and anti-cholinesterase activity of Spanish EVOO have not been as

32 Tissues were also stained for Abeta and cholinesterase activity to visualize Abeta plaque load f

33 Each retained cholinesterase activity with butyrylthiocholine as subst

34 f exposure and well after the restoration of cholinesterase activity.

35 AD brain tissues in which Abeta plaques had cholinesterase activity.

36 survival-forest analysis identified baseline cholinesterase and bilirubin as the most important varia

37 ealed a strong predictive value for baseline cholinesterase and bilirubin levels with a highly nonlin

38 New blood markers, such as serum cholinesterase and inflammatory cytokines, have been int

39 ethyl)prop-2-yn-1-amine (2, MBA236) as a new cholinesterase and monoamine oxidase dual inhibitor.

40 The extracts exerted weak cholinesterase and tyrosinase inhibition, and remarkable

41 tracellular domain with sequence homology to cholinesterases and include the neuroligins, synaptic ce

42 nerve agents are potent toxins that inhibit cholinesterases and produce a rapid and lethal cholinerg

43 to the human liver CE, hCE1, or toward human cholinesterases, and have K(i) values as low as 14 nM.

44 alifornica acetylcholinesterase, recombinant cholinesterases, and monomeric fetal bovine serum acetyl

45 conversely mean aspartate aminotransferase, cholinesterases, and prothrombin time not differed in 2

46 fragment was selected for its inhibition of cholinesterases, and the flavonoid scaffold derived from

47 vel series of optically active inhibitors of cholinesterase: (-)- and (+)-O-carbamoyl phenols of tetr

48 Cholinesterases are serine hydrolases that can potential

49 The successful application of serum-derived cholinesterases as bioscavengers stems from their relati

50 und herein described, (123)I-PIP, can detect cholinesterases associated with Abeta plaques and can di

51 ts also have Abeta plaques within the brain, cholinesterase-associated plaques are generally less abu

52 dict individual risk from baseline values of cholinesterase, bilirubin, type of primary tumor, age at

53 is unmet need, synthesis and evaluation of a cholinesterase-binding ligand, phenyl 4-(123)I-iodopheny

54 The concept of using cholinesterase bioscavengers for prophylaxis against org

55 In contrast, human or equine butyryl-cholinesterase (BuChE) converted CPT-11 to SN-38 with K(

56 overall structure of NL2A resembles that of cholinesterases, but several structural features are uni

57 , a highly potent, irreversible inhibitor of cholinesterase, causes intense convulsions, neuropatholo

58 e cholinergic system (i.e., cerebrum, plasma cholinesterases; cerebrum muscarinic, nicotinic receptor

59 the remaining intact cholinergic cells with cholinesterase (ChE) inhibitors.

60 activators of organophosphate (OP)-inhibited cholinesterases (ChE) was synthesized and tested in vitr

61 Cholinesterases (ChE), use a Glu-His-Ser catalytic triad

62 ity of a new series of oxime reactivators of cholinesterases (ChEs) that contain tertiary amine or im

63 present study, the interaction of E2020 with cholinesterases (ChEs) with known sequence differences,

64 r p 1 level, hepatitis A seropositivity, and cholinesterase concentration on risk of wheeze, and the

65 s unrelated to hepatitis A seropositivity or cholinesterase concentration.

66 Tissues containing a mixture of cholinesterases could be assayed for amount of G117H BCh

67 However, the circulatory stability of cholinesterases could not be correlated with the sialic

68 All studied cholinesterases displayed poor affinity for metaproteren

69 29 was the major metabolite and that plasma cholinesterases do not play the primary role in duration

70 ilar to the enzyme acetylcholinesterase, the cholinesterase domain lacks enzymatic activity and funct

71 ynaptic interactions via their extracellular cholinesterase domain with presynaptic neurexins (NRXs).

72 splice insertions (termed A and B) in the NL cholinesterase domain.

73 peutics such as oximes cannot reactivate the cholinesterase enzyme and relieve cholinergic inhibition

74 e action of tolserine (5) to favor a lack of cholinesterase enzyme subtype selectivity.

75 n situ hybridization histochemistry to study cholinesterase expression during embryogenesis.

76 SIB-1553A did not inhibit rat brain cholinesterase for up to 1 mM.

77 e, in part, for the multiphasic clearance of cholinesterases from the circulation of mice.

78 ies, including P450 monooxygenases, carboxyl/cholinesterases, glutathione-S-transferases, and ATP-bin

79 Radiolabeled ligands specific for cholinesterases have potential for use in neuroimaging A

80 of Alzheimer's disease were processed using cholinesterase histochemistry in the presence or absence

81 The glycans of tetrameric forms of plasma cholinesterases (human serum butyrylcholinesterase, feta

82 Activities of serum cholinesterase in fetal bovine serum and human serum wer

83 ic functions has also been demonstrated with cholinesterase in wet blood.

84 carbohydrate structure and the stability of cholinesterases in circulation, we determined the monosa

85 assays can be used to identify OP-resistant cholinesterases in culture medium and in animal tissues.

86 evelopmental and toxicological influences on cholinesterases in multiple microscopic regions of the r

87 Optimum staining for cholinesterases in neurons and axons was obtained at pH

88 se inhibitors tested, rivastigmine inhibited cholinesterases in normal and pathological structures wi

89 butyrylcholinesterase activities, to inhibit cholinesterases in plaques and tangles.

90 Cholinesterases in plaques, tangles and glia were staine

91 ific mechanistic cascade contributing to the cholinesterase-independent developmental neurotoxicant a

92 with verbal memory recall; and that central cholinesterase inhibition (ChI) would modulate this, imp

93 ystemic illness, such as that resulting from cholinesterase inhibition by organophosphate pesticides.

94 Since previous studies have shown that cholinesterase inhibition enhances visual extrastriate c

95 The clinical relevance of the benefits of cholinesterase inhibition remains controversial, and lon

96 Currently available cholinesterase inhibition therapy targets the cognitive

97 rine revealed no sign that carbamate-induced cholinesterase inhibition was readily reversed in vitro.

98 Cholinesterase inhibition with tacrine appears to reduce

99 ugh chlorpyrifos exerts some effects through cholinesterase inhibition, recent studies suggest additi

100 rce the need to examine endpoints other than cholinesterase inhibition.

101 ide showed significant regional variation in cholinesterase inhibition.

102 pirically with a placebo-controlled study of cholinesterase inhibition.

103 echanism for functional effects unrelated to cholinesterase inhibition.

104 Phenserine, a recently developed cholinesterase inhibitor (ChEI), has been reported to re

105 Therefore, use of a cholinesterase inhibitor (ChI) might improve cognitive f

106 Administration of a central cholinesterase inhibitor (ChI) partially restored the su

107 Cholinesterase inhibitor (ChI) therapy for mixed dementi

108 We show that a brief treatment with the cholinesterase inhibitor aldicarb induces a form of pres

109 Pharmacological assays using the cholinesterase inhibitor aldicarb suggest that VAs and G

110 d to determine the effects of galantamine, a cholinesterase inhibitor and a nicotinic allosteric pote

111 cluding a phenserine analogue as a potential cholinesterase inhibitor and constrained tryptamine deri

112 y measured the effects of treatment with the cholinesterase inhibitor and nicotinic receptor modulato

113 Short-term treatment with a cholinesterase inhibitor appears to enhance the activity

114 he brains of healthy human subjects with the cholinesterase inhibitor donepezil (trade name: Aricept)

115 zed by fusing the pharmacophoric features of cholinesterase inhibitor donepezil and diarylthiazole as

116 found that cholinergic enhancement with the cholinesterase inhibitor donepezil improved target detec

117 The cholinesterase inhibitor donepezil was administered to n

118 Cholinesterase inhibitor drugs improve cognition and neu

119 um samples from individuals asymptomatic for cholinesterase inhibitor exposure were analyzed using th

120 r a psychopharmacological challenge with the cholinesterase inhibitor galantamine (Reminyl).

121 trials of memantine in patients receiving a cholinesterase inhibitor have been performed.

122 ver, a combination of an M2 antagonist and a cholinesterase inhibitor may reach the maximal disease-m

123 The cholinesterase inhibitor methyl paraoxon significantly d

124 with NAC in combination with the peripheral cholinesterase inhibitor neostigmine showed prolonged su

125 In the presence of the cholinesterase inhibitor neostigmine, EFS led to an addi

126 Central Register and/or by prescription of a cholinesterase inhibitor or memantine hydrochloride from

127 cision to initiate a trial of therapy with a cholinesterase inhibitor or memantine on individualized

128 However, the administration of neither the cholinesterase inhibitor physostigmine nor the benzodiaz

129 We studied the effect of the cholinesterase inhibitor physostigmine on subcomponents

130 ith age, and attenuation by the nonselective cholinesterase inhibitor physostigmine, but no attenuati

131 artially susceptible to improvement with the cholinesterase inhibitor physostigmine.

132 Whether a cholinesterase inhibitor should be used as augmentation

133 rophosphate (DCP), a model organophosphorous cholinesterase inhibitor simulant.

134 t dimethoxybenzilidene anabaseine (DMXB) and cholinesterase inhibitor tetrahydroaminoacridine (THA) w

135 We tested the premise that cholinesterase inhibitor therapy should target butyrylch

136 ia responds poorly to nonpharmacological and cholinesterase inhibitor therapy, and although corticost

137 Galantamine, a cholinesterase inhibitor used in Alzheimer's disease, si

138 ucted to assess the impact of galantamine, a cholinesterase inhibitor with nicotinic-receptor-modulat

139 Physostigmine (a centrally active cholinesterase inhibitor) also dose-dependently inhibite

140 while neostigmine (a peripherally restricted cholinesterase inhibitor) did not.

141 rior administration of muscarinic agonist or cholinesterase inhibitor) produced robust but transient

142 have an exaggerated paralytic response to a cholinesterase inhibitor, aldicarb.

143 In contrast, a cholinesterase inhibitor, eserine, although significantl

144 ceptor (mAChR) agonist, oxotremorine, or the cholinesterase inhibitor, neostigmine (NEOS), in the rRP

145 te administration of rivastigmine, a central cholinesterase inhibitor, on patterns of brain activatio

146 from our laboratory have shown that a novel cholinesterase inhibitor, phenserine, reduces betaAPP le

147 Donepezil, a cholinesterase inhibitor, restored performance in animal

148 Rivastigmine, a cholinesterase inhibitor, was tested in a group of clini

149 effects of metrifonate, a second generation cholinesterase inhibitor, were examined on CA1 pyramidal

150 and were treated for at least 1 month with a cholinesterase inhibitor.

151 vention patients were more likely to receive cholinesterase inhibitors (79.8% vs 55.1%; P = .002) and

152 nd visual) were also affected in MCI and (2) cholinesterase inhibitors (ChEIs), one of the therapies

153 Known adverse events of cholinesterase inhibitors (nausea, vomiting, anorexia) w

154 lzheimer's dementia is commonly treated with cholinesterase inhibitors [4-7]; however, these are mode

155 tter addressed by multifunctional drugs than cholinesterase inhibitors alone.

156 mal limb muscles, response to treatment with cholinesterase inhibitors and 3,4-diaminopyridine, and t

157 er of direct acting muscarinic agonists, two cholinesterase inhibitors and a putative m1 agonist/musc

158 Cholinesterase inhibitors and corticosteroids have been

159 Cholinesterase inhibitors and memantine do not have regu

160 for randomised, placebo-controlled trials on cholinesterase inhibitors and memantine in patients with

161 sess the evidence for efficacy and safety of cholinesterase inhibitors and memantine in vascular deme

162 Cholinesterase inhibitors and memantine produce small be

163 Cognitive enhancing drugs, such as cholinesterase inhibitors and methylphenidate, are used

164 ortant implications for the long-term use of cholinesterase inhibitors and other cholinomimetics in t

165 Evidence regarding the benefits of cholinesterase inhibitors and other therapeutic options

166 ning the interaction between carbamate-based cholinesterase inhibitors and their enzyme target.

167 cotinic cholinergic agonists are used, or if cholinesterase inhibitors are combined with other agents

168 Cholinesterase inhibitors are commonly used to improve c

169 results from randomized controlled trials of cholinesterase inhibitors are conflicting.

170 More effective treatments than cholinesterase inhibitors are needed for Alzheimer's dis

171 erate clinically detected Alzheimer disease, cholinesterase inhibitors are somewhat effective in slow

172 Cholinesterase inhibitors are the primary treatment for

173 , and fewer than 20% of patients stop taking cholinesterase inhibitors because of side effects.

174 ifos and diazinon are bioactivated to potent cholinesterase inhibitors by cytochrome P-450 systems.

175 results indicate that one mechanism by which cholinesterase inhibitors can improve memory is by enhan

176 In persons with MCI, cholinesterase inhibitors did not reduce dementia risk (

177 Clinical trials have shown the benefits of cholinesterase inhibitors for the treatment of mild-to-m

178 magnetic scavenging technique for extracting cholinesterase inhibitors from aqueous matrixes using bi

179 These results indicate that cholinesterase inhibitors have a modest beneficial impac

180 PSP, but trials of cholinergic agonists and cholinesterase inhibitors have failed to show improvemen

181 Cholinesterase inhibitors improve attention, as well as

182 Cholinesterase inhibitors improve cognitive outcomes in

183 ompared with placebo, patients randomized to cholinesterase inhibitors improved 0.1 SDs on ADL scales

184 ompared with placebo, patients randomized to cholinesterase inhibitors improved 1.72 points on the NP

185 treatment effects associated with the use of cholinesterase inhibitors in these populations.

186 Treatment with cholinesterase inhibitors is well tolerated by most pati

187 h cognitive and behavioral disturbances, and cholinesterase inhibitors may improve behavior in Alzhei

188 Our findings suggest that treatment with cholinesterase inhibitors may improve muscle function in

189 Cholinesterase inhibitors may improve symptoms of dement

190 Six to 12 months of treatment with cholinesterase inhibitors modestly slows the decline of

191 ny patients' preference to take memantine or cholinesterase inhibitors off-label rather than particip

192 Concomitant treatment with cholinesterase inhibitors or memantine was permitted.

193 The effect of cholinesterase inhibitors or other treatments on persons

194 Cholinesterase inhibitors positively affect cognition in

195 Cholinesterase inhibitors produce small improvements in

196 The cholinesterase inhibitors rivastigmine, donepezil, and m

197 Unlike other cholinesterase inhibitors tested, rivastigmine inhibited

198 The use of cholinesterase inhibitors to correct the cholinergic def

199 ddition, we need to know when to switch from cholinesterase inhibitors to memantine or when to co-pre

200 blocking drugs and encapsulates them, making cholinesterase inhibitors unnecessary.

201 preservation of the cholinergic system (via cholinesterase inhibitors) and hippocampal neurons (via

202 organophosphorus compounds (OPs) are potent cholinesterase inhibitors, accounting for their use as i

203 Antipsychotics, cholinesterase inhibitors, and alpha-2 agonists are the

204 , diarrhoea, and insomnia) occurred with the cholinesterase inhibitors, but not with memantine.

205 Stable use of cholinesterase inhibitors, estrogen, low-dose aspirin, a

206 The cholinesterase inhibitors, tacrine and physostigmine, an

207 ly accessible both for the substrate and for cholinesterase inhibitors.

208 in locomotion behavior and responsiveness to cholinesterase inhibitors.

209 onsidered, concentrating upon studies of the cholinesterase inhibitors.

210 was no difference in efficacy among various cholinesterase inhibitors.

211 ntine or when to co-prescribe memantine with cholinesterase inhibitors.

212 orted by an improvement of these symptoms by cholinesterase inhibitors.

213 detection of organophosphates or exposure to cholinesterase inhibitors.

214 rase system, and achieve effective dual FAAH/cholinesterase inhibitors.

215 r is as a promising new tool for analysis of cholinesterase inhibitors.

216 erred both acetyl (AChE) and butyryl (BuChE) cholinesterase inhibitory activities at similar concentr

217 ric forms of each series demonstrated potent cholinesterase inhibitory activity (with IC(50) values a

218 In contrast to their potent cholinesterase inhibitory activity, all of the pyridophe

219 ing excellent antioxidant properties, strong cholinesterase inhibitory activity, less hepatotoxicity

220 e of five tissue-derived and two recombinant cholinesterases (injected intravenously in mice) with th

221 Moreover, their inhibition of cholinesterase is of interest regarding neurodegenerativ

222 RIC-3 (resistant to inhibitor of cholinesterase) is a transmembrane protein, found in inv

223 the continuous variables bilirubin level and cholinesterase level was determined.

224 Similarly, cholinesterase levels below 7.5 U predicted a strong inc

225 es a structural basis for design of improved cholinesterase ligands for treating Alzheimer's disease

226 shown by proton NMR that horse serum butyryl cholinesterase, like serine proteases, forms a short, st

227 roximately 720 residues), and the C-terminal cholinesterase-like (ChEL) domain ( approximately 570 re

228 sidues); regions II-III (~720 residues); and cholinesterase-like (ChEL) domain (~570 residues).

229 The carboxyl-terminal cholinesterase-like (ChEL) domain of thyroglobulin (Tg)

230 llectively as region I-II-III) followed by a cholinesterase-like (ChEL) domain.

231 I, followed by the approximately 570 residue cholinesterase-like (ChEL) domain.

232 ide new evidence that authentic AChE and the cholinesterase-like domain of Tg share a common tertiary

233 ociate with neuroligins (a related family of cholinesterase-like proteins), demonstrating potential f

234 we find that a Tg truncation, deleted of the cholinesterase-like region (but not a comparably sized d

235 atalytically inactive members of a family of cholinesterase-like transmembrane proteins that mediate

236 Concerning cholinesterases, LP was the most active, mainly due to l

237 recent histological studies using the acetyl cholinesterase method and also a more definitive techniq

238 choline acetyltransferase mRNA and decreased cholinesterase mRNAs.

239 arbolinium salts as potent inihitors of both cholinesterases, N-methyl-D-aspartate receptors, and mon

240 n mRNA levels of the related enzyme, butyryl-cholinesterase, nor of the high-affinity choline transpo

241 orous acid), and inhibitory activity against cholinesterase of the new blend were determined and comp

242 The effects of the anti-cholinesterase organophosphate pesticide chlorpyrifos (C

243 mechanism of dealkylation in soman-inhibited cholinesterases proposed previously.

244 symmetrization of meso-diacetate with acetyl cholinesterase, radical cyclization, and Lewis acid-cata

245 ar interstitial cells of Cajal (ICC-IMs) and cholinesterases restrict ACh accessibility to a select p

246 We suggest that the high catalytic power of cholinesterases results in part from the formation of a

247 Amino acid sequence alignments of cholinesterases revealed that 6 of 14 aromatic amino aci

248 1 genes, that are resistant to inhibitors of cholinesterase (Ric mutants).

249 Resistance to inhibitors of cholinesterase (Ric) 8A is a guanine nucleotide exchange

250 Resistance to inhibitors of cholinesterase (Ric-8)A and Ric-8B are essential genes t

251 erences in the pharmacokinetic parameters of cholinesterases seem to be due to the combined effect of

252 ed almost entirely by measurements of acetyl cholinesterase, size, and ploidy without concomitant ass

253 howed that the decrease in the percentage of cholinesterase-stained zones (CSZ) exhibiting nerve term

254 act with the synaptic basal lamina marked by cholinesterase staining even in the absence of the targe

255 e conclusions were later supported by acetyl cholinesterase staining using a method that appeared not

256 posed endocannabinoid system and the classic cholinesterase system, and achieve effective dual FAAH/c

257 similarity in structure and function to the cholinesterase targets of nerve agent poisoning.

258 c overactivity and NMJ Ca(2+) overload, anti-cholinesterase toxicity and the slow-channel myasthenic

259 Cholinesterases use a Glu-His-Ser catalytic triad to enh

260 The effect on the cholinesterases was not as strong as in previous reports

261 role of glycosylation in the circulation of cholinesterases, we compared the mean residence time of

262 Wild-type cholinesterases were completely inhibited by 0.1 mM echo

263 Mild effects on cholinesterases were observed with the certified samples

264 emporally regulated ganglionic expression of cholinesterases, which may be important in the developme

265 These pathological cholinesterases, with altered properties, are suggested

266 kely to result in inhibition of pathological cholinesterases, with the potential of interfering with

267 spatiotemporal change in expression of each cholinesterase within the DRG.