ライフサイエンスコーパス: N-methyl

1 The reaction of N-methyl-1,2,4-triazoline-3,5-dione (MeTAD) with anisole

2 e (11)C-labeled conjugated bile acid analog [N-methyl-(11)C]cholylsarcosine ((11)C-CSar).

3 ward this end, we developed protocols for 2'-N-methyl-2'-amino-2'-deoxyuridine phosphoramidites that

4 5-(aminosulfonyl)-4-methyl-1,3-thiazol-2-yl]-N-methyl-2-[4-(2-pyridinyl)phenyl ]acetamide, a helicase

5 vigorously with the standard slurry solvent N-methyl-2-pyrrolidinone (NMP), indicating it is not com

6 g the ratio between organic solvents such as N-methyl-2-pyrrolidinone or ortho-dichlorobenzene, and n

7 ow the molecular size and chemical nature of N-methyl-2-pyrrolidone (NMP) give rise to the chiral tra

8 N-methyl-2-pyrrolidone (NMP) has been shown to be the mo

9 ays, the common agrochemical inert formulant N-methyl-2-pyrrolidone (NMP) is at least 20 times more t

10 organic liquids (acetone, ethanol, methanol, N-methyl-2-pyrrolidone (NMP), carbon tetrachloride and w

11 tin(II) sulfide to produce SnS nanosheets in N-methyl-2-pyrrolidone is reported.

12 dimethylformamide, N,N-dimethylacetamide and N-methyl-2-pyrrolidone), and without the need for a cata

13 failure has produced a series of substituted N-methyl-3-(pyrimidin-4-ylamino)benzenesulfonamide inhib

14 ntification of a promising anolyte material, N-methyl 4-acetylpyridinium tetrafluoroborate.

15 N-methyl 4-MA was an efficacious substrate-type releaser

16 ceeded (>72%) through demethylation yielding N-methyl-4-cyanoaniline and formaldehyde as primary prod

17 end, monkeys were rendered parkinsonian with n-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) and

18 With water-soluble iron tetrakis(N-methyl-4-pyridyl)porphyrin as an example, procedures a

19 commercial chromophore E-4'-(dimethylamino)-N-methyl-4-stilbazolium.

20 the synthesis of unsymmetrically substituted N-methyl/alkyl anilines through a direct three-component

21 a second heptapeptide sequence containing an N-methyl amino acid.

22 alinoyltetramic acid (-)-hymenosetin and its N-methyl analogue were prepared in 11 and 8 steps, respe

23 employed along with a strategic placement of N-methyl and d-amino acids to produce passively permeabl

24 N-methyl and N-ethyl 4-MA were substrates at NET, wherea

25 ing optically active 2-benzyl morpholine and N-methyl camphanyl piperazine.

26 Furthermore, the N-methyl compound (+)-15a, which displayed an EC50 of 23

27 d NMR correlations, we have identified novel N-methyl-containing amines and amides, primary amides, a

28 opposes synaptic strengthening by increasing N-methyl D-aspartate glutamate receptor (NMDAR) internal

29 th MoCD, and demonstrated that it acts as an N-methyl D-aspartate receptor (NMDA-R) agonist, leading

30 n for ketamine is mediated primarily through N-methyl d-aspartate receptor (NMDAR) antagonism; howeve

31 NSFT following EtOH abstinence utilizing the N-methyl D-aspartate receptor (NMDAR) antagonist and ant

32 Anti-N-methyl D-aspartate receptor (NMDAR) encephalitis is a

33 The activation of the N-methyl D-aspartate receptor (NMDAR) is controlled by a

34 KYNA depletion then leads, in an N-methyl D-aspartate receptor (NMDAR)-dependent manner,

35 findings demonstrate the epileptogenicity of N-methyl D-aspartate receptor antibodies in vivo, and su

36 r bound to compound 1 (Cmpd-1), a novel A2AR/N-methyl d-aspartate receptor subtype 2B (NR2B) dual ant

37 opioid facilitation, and interactions of the N-methyl D-aspartate receptor with opioids at the level

38 d-Serine modulates N-methyl d-aspartate receptors (NMDARs) and regulates sy

39 st-mortem, surprisingly, the total number of N-methyl D-aspartate receptors did not differ between te

40 in G either reduced synaptic localization of N-methyl D-aspartate receptors, or had a direct effect o

41 Most patients with N-methyl D-aspartate-receptor antibody encephalitis deve

42 ing decreases in tyrosine phosphorylation of N-methyl-D aspartate (NMDA) receptor subunit 2 (GluN2) t

43 ring wakefulness and are also induced in the N-methyl-D-asparate receptor hypofunction rat model.

44 a-aminobutyric acid A receptor activation or N-methyl-d-asparate receptor inhibition but were associa

45 of SFK targets, including GluN2A and GluN2B N-methyl-D-aspartate (NMDA) and GluA2 alpha-amino-3-hydr

46 In healthy subjects (HS), N-methyl-D-aspartate (NMDA) antagonists like memantine a

47 roduce low frequency tonic firing results in N-methyl-D-aspartate (NMDA) excitation balanced by gamma

48 suggests that ketamine, an antagonist of the N-methyl-d-aspartate (NMDA) glutamate receptor (GluR), h

49 In vivo imaging of N-methyl-d-aspartate (NMDA) glutamate receptor and gamma

50 novel glutamatergic compound that acts as an N-methyl-D-aspartate (NMDA) modulator with glycine-like

51 -methyl-4-isoxazole propionic acid (AMPA) to N-methyl-D-aspartate (NMDA) ratios, and matrix metallopr

52 d whether microRNAs (miRNAs) are involved in N-methyl-D-aspartate (NMDA) receptor (NMDAR)-dependent A

53 synapse function and plasticity, especially N-methyl-d-aspartate (NMDA) receptor (NMDAR)-dependent l

54 pendent on the time interval between spikes, N-methyl-D-aspartate (NMDA) receptor activation, and Cal

55 The glutamate N-methyl-D-aspartate (NMDA) receptor antagonist ketamine

56 Antidepressant activity of N-methyl-D-aspartate (NMDA) receptor antagonists and neg

57 Pretreatment with N-methyl-D-aspartate (NMDA) receptor antagonists AP5 and

58 N-methyl-D-aspartate (NMDA) receptor antagonists have be

59 view and meta-analysis of ketamine and other N-methyl-d-aspartate (NMDA) receptor antagonists in the

60 urons and cell-based assays to test for anti-N-methyl-d-aspartate (NMDA) receptor antibodies.

61 dine) has been used successfully to quantify N-methyl-d-aspartate (NMDA) receptor binding in humans.

62 Although N-methyl-d-aspartate (NMDA) receptor blockade stabilizes

63 ions in the DP were significantly reduced by N-methyl-d-aspartate (NMDA) receptor blockade.

64 N-Methyl-d-aspartate (NMDA) receptor dysfunction has bee

65 preclinical research with modulators at the N-methyl-d-aspartate (NMDA) receptor GluN2B N-terminal d

66 N-methyl-d-aspartate (NMDA) receptor ion channel is acti

67 the phencyclidine (PCP) binding site of the N-methyl-d-aspartate (NMDA) receptor or with sigma1 rece

68 Recent work highlights a role for altered N-methyl-d-aspartate (NMDA) receptor signaling and relat

69 wal may be due to glutamate toxicity, as the N-methyl-d-aspartate (NMDA) receptor subunit NR2B was up

70 The role of the glutamatergic N-methyl-D-aspartate (NMDA) receptor system in hedonic f

71 For we believe the first time, we show that N-methyl-d-aspartate (NMDA) receptor-dependent Ca(2+) tr

72 Evoked, N-methyl-D-aspartate (NMDA) receptor-mediated currents w

73 pal neurons, calcium ion (Ca2+) flux through N-methyl-D-aspartate (NMDA) receptors activates Ca2+/cal

74 renic motoneuron expression of glutamatergic N-methyl-D-aspartate (NMDA) receptors and decreased expr

75 N-methyl-d-aspartate (NMDA) receptors are expressed thro

76 N-methyl-D-aspartate (NMDA) receptors are glutamate- and

77 N-methyl-d-aspartate (NMDA) receptors are glutamate- and

78 N-Methyl-D-aspartate (NMDA) receptors are glutamate-gate

79 The N-methyl-d-aspartate (NMDA) receptors are heteromeric no

80 N-methyl-d-aspartate (NMDA) receptors are ligand-gated,

81 taken together with the strong expression of N-methyl-D-aspartate (NMDA) receptors by its cells, are

82 Activation of extrasynaptic N-methyl-d-aspartate (NMDA) receptors causes neurodegene

83 A distinctive characteristic of N-methyl-D-aspartate (NMDA) receptors containing a GluN2

84 genetic approaches, we find that ablation of N-methyl-D-aspartate (NMDA) receptors during postnatal d

85 Hypofunction of N-methyl-d-aspartate (NMDA) receptors has been proposed

86 Competitive antagonists against N-methyl-D-aspartate (NMDA) receptors have played critic

87 it has been postulated that hypofunction of N-methyl-d-aspartate (NMDA) receptors in brain networks

88 The physiology of N-methyl-d-aspartate (NMDA) receptors is fundamental to

89 ry that ketamine, an antagonist of glutamate/N-methyl-D-aspartate (NMDA) receptors, elicits antidepre

90 citotoxicity, mediated by overstimulation of N-methyl-D-aspartate (NMDA) receptors, is a mechanism th

91 lutamate release activating Ca(2+)-permeable N-methyl-D-aspartate (NMDA) receptors.

92 -induced downregulation of GluN2B-containing N-methyl-D-aspartate (NMDA) receptors.

93 has been successfully used in PET imaging of N-methyl-d-aspartate (NMDA) receptors.

94 -methyl-4-isoxazolepropionic acid (AMPA) and N-methyl-D-aspartate (NMDA) receptors.

95 ne implicated in influencing learning is the N-methyl-D-aspartate (NMDA) subtype 2B glutamate recepto

96 s was mediated by glutamate receptors of the N-methyl-d-aspartate (NMDA) subtype and resulted in remo

97 The N-methyl-d-aspartate (NMDA) subtype of the ionotropic gl

98 ceptor (iGluR) agonists, kainic acid (KA) or N-methyl-D-aspartate (NMDA), contributed to significant,

99 traocular) unimNPs with the glutamate analog N-methyl-d-aspartate (NMDA), which is excito-toxic and i

100 tive confocal immunofluorescence showed that N-methyl-D-aspartate (NMDA)-receptor labeling was presen

101 e quantitated the cell surface expression of N-methyl-D-aspartate (NMDA)-type and alpha-amino-3-hydro

102 N-methyl-d-aspartate (NMDA)-type ionotropic glutamate re

103 clear whether d-cycloserine (DCS), a partial N-methyl-d-aspartate agonist that enhances fear extincti

104 d-cycloserine (DCS), a partial glutamatergic N-methyl-D-aspartate agonist, as an augmentation strateg

105 apentinoids, tramadol, lidocaine, and/or the N-methyl-d-aspartate class of glutamate receptor antagon

106 methyl-4-isoxazole propionic acid (AMPA) and N-methyl-D-aspartate currents and the ability to exhibit

107 iation at these synapses as measured by AMPA/N-methyl-D-aspartate currents.

108 ysfunction is further posited to result from N-methyl-D-aspartate glutamate receptor (NMDAR) hypofunc

109 Ketamine, an N-methyl-d-aspartate glutamate receptor antagonist, has

110 rapid antidepressant effects of ketamine, an N-methyl-D-aspartate glutamate receptor antagonist, have

111 At subanesthetic doses, ketamine, an N-methyl-D-aspartate glutamate receptor antagonist, incr

112 als and humans, particularly those involving N-methyl-D-aspartate glutamate receptor antagonists, to

113 izophrenia is associated with disruptions in N-methyl-D-aspartate glutamate receptor subtype (NMDAR)-

114 astric tone and motility were recorded after N-methyl-d-aspartate microinjection in the SNpc and/or o

115 ommissural pathways mimicking the effects of N-methyl-D-aspartate on locomotor frequency in isolated

116 e subset of antibody-positive patients, anti-N-methyl-d-aspartate receptor (5 patients), had normal M

117 vated protein 1 [LGI1] Ab), and 4 (3.6%) had N-methyl-D-aspartate receptor (NMDAR) Ab.

118 Increased N-methyl-d-aspartate receptor (NMDAR) activity in the pa

119 F2K) activity subsequent to the reduction in N-methyl-D-aspartate receptor (NMDAR) activity.

120 We recorded N-methyl-D-aspartate receptor (NMDAR) and alpha-amino-3-

121 de registers to search for antibodies to the N-methyl-D-aspartate receptor (NMDAR) and contactin-asso

122 von Frey filaments to examine the roles that N-methyl-D-aspartate receptor (NMDAR) and hyperpolarizat

123 The psychotomimetic effect of the N-methyl-D-aspartate receptor (NMDAR) antagonist ketamin

124 tamine, a non-competitive, voltage-dependent N-Methyl-D-aspartate receptor (NMDAR) antagonist, has be

125 Through the fortuitous discovery of N-methyl-D-aspartate receptor (NMDAR) antagonists as eff

126 A single injection of N-methyl-D-aspartate receptor (NMDAR) antagonists produc

127 Similar to mice treated chronically with N-methyl-d-aspartate receptor (NMDAR) antagonists, we de

128 RATIONALE: Encephalitis caused by anti-N-methyl-d-aspartate receptor (NMDAR) antibodies is the

129 ot alter the density of excitatory synapses, N-methyl-D-aspartate receptor (NMDAR) clusters, or cell

130 The N-methyl-D-aspartate receptor (NMDAR) coagonists glycine

131 The N-methyl-d-aspartate receptor (NMDAR) controls synaptic

132 ly overlooked in schizophrenia research, and N-methyl-d-aspartate receptor (NMDAR) dysfunction can pr

133 The majority of patients with anti-N-methyl-D-aspartate receptor (NMDAR) encephalitis suffe

134 normal in the majority of patients with anti-N-methyl-D-aspartate receptor (NMDAR) encephalitis.

135 Mutations in the N-methyl-D-aspartate receptor (NMDAR) gene GRIN2A cause

136 ulating autoantibodies against glutamatergic N-methyl-D-aspartate receptor (NMDAR) have been reported

137 N-methyl-D-aspartate receptor (NMDAR) hypofunction in pa

138 s glutamate excess in schizophrenia and that N-methyl-d-aspartate receptor (NMDAR) hypofunction on ga

139 The N-methyl-D-aspartate receptor (NMDAR) is a member of the

140 Abnormal activity of various N-methyl-d-aspartate receptor (NMDAR) subtypes has been

141 Early postnatal experience shapes N-methyl-D-aspartate receptor (NMDAR) subunit compositio

142 ncoded by GRIN2A and GRIN2B) subunits of the N-methyl-D-aspartate receptor (NMDAR), a ligand-gated io

143 able samples were retested for antibodies to N-methyl-d-aspartate receptor (NMDAR), the glycine recep

144 ansmitter molecules, is its manifestation as N-methyl-d-aspartate receptor (NMDAR)-dependent slow inw

145 associations is known to rely on hippocampal N-methyl-D-aspartate receptor (NMDAR)-dependent synaptic

146 impairments are thought to be due to reduced N-methyl-D-aspartate receptor (NMDAR)-mediated inhibitio

147 and are linked to underlying dysfunction of N-methyl-D-aspartate receptor (NMDAR)-mediated neurotran

148 In particular, a robust decrease in N-methyl-D-aspartate receptor (NMDAR)-mediated synaptic

149 antibodies-especially antibodies against the N-methyl-D-aspartate receptor (NMDAR)-more commonly than

150 llosteric antagonists of ion channels of the N-methyl-d-aspartate receptor (NMDAR).

151 cytoskeleton-associated protein (P=0.23) or N-methyl-D-aspartate receptor (P=0.74) post-synaptic sig

152 nses in CA2 pyramidal neurons that relied on N-methyl-d-aspartate receptor activation and calcium/cal

153 N-methyl-D-aspartate receptor activation requires the bi

154 , including acetylcholinesterase inhibition, N-methyl-D-aspartate receptor activation, and calcium dy

155 The findings implicate dysfunction of N-methyl-D-aspartate receptor and glutamatergic neurotra

156 The N-methyl-D-aspartate receptor antagonist ketamine can im

157 suggests a single sub-anesthetic dose of the N-methyl-D-aspartate receptor antagonist ketamine may wo

158 influx that can be partially blocked by the N-methyl-d-aspartate receptor antagonist MK-801.

159 Ketamine is a potent N-methyl-D-aspartate receptor antagonist with a potentia

160 of inflammatory genes, and that ketamine (an N-methyl-D-aspartate receptor antagonist) would reduce o

161 Ketamine is an N-methyl-D-aspartate receptor antagonist, which on admin

162 Additionally, the NR2B-selective N-methyl-D-aspartate receptor antagonists ifenprodil and

163 N-methyl-D-aspartate receptor antagonists, such as ketam

164 ody testing confirmed identification of anti-N-methyl-D-aspartate receptor antibodies in the cerebros

165 There are now a large number of requests for N-methyl-D-aspartate receptor autoantibody (NMDAR-Ab) te

166 These data implicate NR2A-related N-methyl-D-aspartate receptor development in adolescent

167 hizophrenia thought to reflect glutamatergic N-methyl-d-aspartate receptor function and excitatory-in

168 Inhibition of neuronal activity, N-methyl-d-aspartate receptor function, or glycogen synt

169 abnormal glutamateric neurotransmission and N-methyl-D-aspartate receptor hypofunction in the pathop

170 The N-methyl-D-aspartate receptor hypofunction model of schi

171 nts, glycine receptor (GLY-R) in 5 patients, N-methyl-d-aspartate receptor in 4 patients and gamma-am

172 chosis patients (3 IgG, 1 IgM, 0 IgA) and to N-methyl-D-aspartate receptor in 6 of 43 patients (5 IgG

173 d-cycloserine, a partial agonist at the N-methyl-d-aspartate receptor in the amygdala, has been

174 pression of the essential NR1 subunit of the N-methyl-D-aspartate receptor increased during downstrea

175 r gamma-aminobutyric acid type A receptor or N-methyl-D-aspartate receptor inhibition.

176 ications for understanding D-serine-mediated N-methyl-D-aspartate receptor plasticity in the amygdala

177 inct subdivisions of ACC with different AMPA/N-methyl-D-aspartate receptor profiles.

178 gic synapses, particularly components of the N-methyl-D-aspartate receptor signaling complex, includi

179 d number of key synaptic proteins, including N-methyl-d-aspartate receptor subunit 2B (NR2B) and PSD-

180 ts, with the GRIN2A gene encoding the GluN2A N-methyl-d-aspartate receptor subunit being most often a

181 Autoantibodies (AB) against N-methyl-D-aspartate receptor subunit NR1 (NMDAR1) are h

182 ing impaired spine pruning and switch in the N-methyl-D-aspartate receptor subunit, which are relevan

183 -hydroxy-5-methyl-4-isoxazole propionic acid/N-methyl-D-aspartate receptor transmission.

184 the stimulated spine that depends on NMDAR (N-methyl-d-aspartate receptor) and CaMKII signalling and

185 The non-competitive, glutamatergic NMDAR (N-methyl-d-aspartate receptor) antagonist (R,S)-ketamine

186 nstrated that this effect was independent of N-methyl-D-aspartate receptor, low-density lipoprotein-r

187 protein-1 (Sp1)-binding site resulted in an N-methyl-d-aspartate receptor-dependent enhancement of C

188 N-methyl-D-aspartate receptor-dependent plasticity in th

189 Here we report that hippocampal N-methyl-d-aspartate receptor-dependent synaptic plastic

190 tatory synaptic activity and was shown to be N-methyl-d-aspartate receptor-dependent.

191 most common and was predicted best when both N-methyl-D-aspartate receptor-IgG and aquaporin-4-IgG co

192 amine is a non-competitive antagonist at the N-methyl-d-aspartate receptor.

193 N-Methyl-D-aspartate receptors (NMDA-Rs) are ion channel

194 ifferences in the pharmacological profile of N-methyl-d-aspartate receptors (NMDAR) in the NAc core,

195 PS modulates N-methyl-D-aspartate receptors (NMDARs) and has been sho

196 n interaction between synaptic activation of N-methyl-D-aspartate receptors (NMDARs) and intrinsic os

197 quivocal uncompetitive inhibitory effects on N-methyl-d-aspartate receptors (NMDARs) and may preferen

198 t synaptic accumulation of GluN2B-containing N-methyl-D-aspartate receptors (NMDARs) and pathological

199 N-methyl-D-aspartate receptors (NMDARs) are glutamate-ga

200 N-methyl-d-aspartate receptors (NMDARs) are glutamate-ga

201 N-Methyl-D-aspartate receptors (NMDARs) are glutamate-ga

202 N-methyl-D-aspartate receptors (NMDARs) are glycoprotein

203 N-methyl-d-aspartate receptors (NMDARs) are heterotetram

204 N-methyl-d-aspartate receptors (NMDARs) are ionotropic g

205 N-methyl-D-aspartate receptors (NMDARs) are ligand-gated

206 N-methyl-D-aspartate receptors (NMDARs) are necessary fo

207 The N-methyl-d-aspartate receptors (NMDARs) constitute an im

208 N-Methyl-d-aspartate receptors (NMDARs) display a critic

209 The significant role played by N-methyl-d-aspartate receptors (NMDARs) in both the path

210 Postsynaptic N-methyl-d-aspartate receptors (NMDARs) phasically activ

211 N-Methyl-D-aspartate receptors (NMDARs) play pivotal rol

212 Synaptic activation of N-methyl-d-aspartate receptors (NMDARs) plays a key role

213 Preclinical studies revealed contribution of N-methyl-D-aspartate receptors (NMDARs) to a variety of

214 Coactivation of N-methyl-D-aspartate receptors (NMDARs) together with AM

215 Alcohol may act on N-methyl-d-aspartate receptors (NMDARs) within cortical

216 SAP102 binds directly to N-methyl-D-aspartate receptors (NMDARs), anchors recepto

217 rine models have shown altered expression of N-methyl-D-aspartate receptors (NMDARs).

218 apse require stimulation of both betaARs and N-methyl-D-aspartate receptors (NMDARs).

219 -isoxazole-propionate receptors (AMPARs) and N-methyl-d-aspartate receptors (NMDARs).

220 stent firing of 'Delay cells' is mediated by N-methyl-d-aspartate receptors and weakened by cAMP-PKA-

221 lpha-syn modulation of the GluN2D-expressing N-methyl-D-aspartate receptors in cholinergic interneuro

222 eleased glutamate that selectively activated N-methyl-d-aspartate receptors in homotypic, but not het

223 N-Methyl-D-aspartate receptors mediate the slow componen

224 Blocking N-methyl-D-aspartate receptors or activation of extracel

225 reas stimulating predominantly extrasynaptic N-methyl-D-aspartate receptors promoted the proteasomal

226 d modulation of extinction and plasticity on N-methyl-D-aspartate receptors was examined as well.

227 as potent inihitors of both cholinesterases, N-methyl-D-aspartate receptors, and monoamine oxidases.

228 tion between alpha-syn and GluN2D-expressing N-methyl-D-aspartate receptors, represents a precocious

229 ations between domain layers, reminiscent of N-methyl-D-aspartate receptors.

230 roxy-5-methyl-4-isoxazole propionic acid and N-methyl-D-aspartate receptors.

231 eltaC synergistically augmented signaling by N-methyl-d-aspartate receptors.

232 t of both alpha7 nicotinic acetylcholine and N-methyl-D-aspartate receptors.

233 y and Rho kinases as well as NR2B-containing N-methyl-D-aspartate receptors.

234 pharmacological manipulation targeted at the N-methyl-D-aspartate type glutamate receptor (NMDAR).

235 genic state in vitro and in vivo after NMDA (N-methyl-d-aspartate) damage in young mice.

236 Furthermore, NMDA (N-methyl-d-aspartate) receptor antagonism by ketamine ha

237 rengthening of synaptic connections by NMDA (N-methyl-d-aspartate) receptor-dependent long-term poten

238 We further identify N-methyl-d-aspartate-dependent long-term depression (NMD

239 N-methyl-d-aspartate-encephalitis or inborn errors of me

240 terious effects are very likely caused by an N-methyl-d-aspartate-mediated non-opioid mechanism as Dy

241 N-methyl-D-aspartate-receptors (NMDARs) are ionotropic g

242 Specifically, an increase in the N-methyl-d-aspartate-type 1 receptor (NMDA-NR1) expressi

243 We found that N-methyl-d-aspartate-type glutamate receptor (NMDAR) act

244 While overstimulation of N-methyl-d-aspartate-type glutamate receptors (NMDARs) i

245 identified subunits required for assembly of N-methyl-d-aspartic acid (NMDA) receptors (NMDA-Rs), alp

246 Blockade of N-methyl-D-aspartic acid (NMDA) receptors by intra-CA3 i

247 In addition to LRP1, we demonstrate that the N-methyl-D-aspartic acid receptor (NMDA-R) is expressed

248 ibited by MK-801, a specific pore blocker of N-Methyl-D-aspartic acid receptor (NMDAR) channels, and

249 By measuring N-methyl-d-aspartic acid receptor (NMDAR)-driven calcium

250 pinal fluid (CSF) levels of the glia-derived N-methyl-D-aspartic acid receptor antagonist kynurenic a

251 passage of larger synthetic cations, such as N-methyl-d-glucamine (NMDG(+)).

252 r by replacement of extracellular Na(+) with N-methyl-d-glucamine.

253 hus, the pathway to the common intermediate, N-methyl-Delta(1)-pyrrolinium, is seen to introduce simi

254 Sarcosine, an N-methyl derivative of the amino acid glycine and a meta

255 uses an aqueous solution of LaCl3.7H2O with N-methyl formamide as porogen and propylene oxide as ini

256 ticularly for site-specific C-H insertion at N-methyl functionalities, offers utility in a range of a

257 inhibitors (SSRIs) such as fluoxetine ((+/-)-N-methyl-gamma-[4-(trifluoromethyl)phenoxy]benzenepropan

258 ckbone H-bond impairing modifications (alpha)N-methyl Gln or l-Pro at key positions within betaHP.

259 escence and excellent photostability, (b) an N-methyl group at each end of the squaraine core that en

260 An N-methyl group at position 33 blocks uncontrolled aggreg

261 -benzo[g]indoles with [1,3] migration of the N-methyl group into the newly formed pyrrole ring; (ii)

262 respectively), proceeds via oxidation of the N-methyl group, resulting in the release of formaldehyde

263 metabolites 11beta-prostaglandinF2alpha and N-methyl histamine (NMH), and bone marrow findings.

264 excretion of 11beta-prostaglandinF2alpha and N-methyl histamine, with serum tryptase, whole blood ser

265 the three-step synthesis of gamma-carboline N-methyl ingenine B.

266 tructural formula of the native L3P as D-Phe-N-Methyl-L-Val-L-Ala-OMe attached in N-ter to a 20-carbo

267 rent cysLT) or the selective CysLT2R agonist N-methyl LTC4 to allergen sensitized wild-type mice mark

268 -4(3H)-ones, a series of potent JmjC histone N-methyl lysine demethylase (KDM) inhibitors which bind

269 hylases (LSDs or KDM1s) and JmjC families of N-methyl-lysine demethylases (JmjC KDMs, KDM2-7), focusi

270 is increasing interest in targeting histone N-methyl-lysine demethylases (KDMs) with small molecules

271 y by employing two GQ-interacting compounds, N-methyl mesoporphyrin IX (NMM) and Crystal Violet (CV).

272 The fluorescent dye, N-Methyl mesoporphyrin IX, binds to these G-quadruplex s

273 uences bind to a G4-binding fluorescent dye, N-methyl-mesoporphyrin IX (NMM).

274 aniline; and for (N-ethoxycarbonylcarbamoyl)(N'-methyl-N'-phenylcarbamoyl)disulfane, which is a short

275 for [1-ethoxy-(N-ethoxycarbonyl)formimidoyl](N'-methyl-N'-phenylcarbamoyl)disulfane, which is obtaine

276 upon the treatment of DNA-methylating agent N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) and antimeta

277 to the prototypic Sn1-type methylating agent N-methyl-N'-nitro-N-nitrosoguanidine.

278 eAN)2Cu(II)2(O2(2-))](2+) ((S)P(MeAN), MeAN: N-methyl-N,N-bis[3-(dimethylamino)propyl]amine) that fea

279 affords functionalization of N-CH3 groups in N-methyl-N,N-dialkylamines with high selectivity over N-

280 1-(2-chlorophenyl)-N-methyl-N-(1-methylpropyl)-3-isoquinolinecarboxamide (P

281 ization reactions have been carried out with N-methyl-N-(tert-butyldimethylsilyl)-trifluoroacetamide

282 ed ditrimethylsilyl (diTMS) species with the N-methyl-N-(trimethylsilyl)-trifluoroacetamide (MSTFA) r

283 temperature, derivatization time and sample: N-methyl-N-(trimethylsilyl)trifluoroacetamide (MSTFA) vo

284 Using N-methyl-N-nitro-N-nitroso-guanidine mutagenesis and sel

285 we demonstrate that the volatile mycotoxin, N-methyl-N-nitrosoisobutyramide, is the dominant factor

286 l, an active component of Cassia seed, in an N-methyl-N-nitrosourea (MNU)-induced mouse model of RP.

287 omarkers related to the consumption of peas (N-methyl nicotinic acid), apples (rhamnitol), and onions

288 The reactions of nitramine, N-methyl nitramine, and N,N-dimethyl nitramine with anhy

289 N-methyl perfluorobutane sulfonamidoacetic acid (MeFBSAA

290 A), perfluorohexanesulfonate (PFHxS), and 2-(N-methyl-perfluorooctane sulfonamido) acetate (Me-PFOSA-

291 Six PFCs [2-(N-methyl-perfluorooctane sulfonamido) acetate (Me-PFOSA-

292 Furthermore, pirenzepine, diphenyl-acetoxy-N-methyl-piperidine and mecamylamine had no measurable e

293 irezenpine; 2 mum) and M3- (diphenyl-acetoxy-N-methyl-piperidine; 100 nm) receptor blockers, but not

294 alkyl chains ranging from C1 to C5 and also N-methyl PQS, yielding the corresponding 2-hydroxy-1,2-d

295 Introduction of an N-methyl protecting group to the ligand inhibits this ox

296 ylsulfonyl)imide ([C2mim][NTf2]) and N-butyl-N-methyl-pyrrolidinium bis(trifluoromethylsulfonyl)imide

297 pression changes, but had lower nicotinamide N-methyl transferase (NNMT) levels and were predisposed

298 We showcase our workflow by annotating N-methyl-uridine monophosphate (UMP), lysomonogalactosyl

299 ese modules would produce the tripeptide Phe-N-Methyl-Val-Ala with a lipid moiety, termed lipotripept

300 , and a naphthalene diimide substituted with N-methyl viologenyl moieties as donor and acceptor monom