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 ex (eta(5)-C(5)Me(5))Rh((Me)PhI)H ((Me)PhI = N-methyl-1-phenylethan-1-imine) exhibited higher thermal

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

4 extended library of differently substituted N-methyl-14- O-methylmorphinans with natural and unnatur

5 ,5-dimethyl-tetrazole, a positive CFG on the N-methyl (2-position) lowers the fragmentation barrier b

6 5-(aminosulfonyl)-4-methyl-1,3-thiazol-2-yl]-N-methyl-2-[4-(2-pyridinyl)phenyl ]acetamide, a helicase

7 We reveal an unusual beta-keto acid (N-methyl-2-aminobenzoylacetate) precursor that is derive

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

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

10 N-methyl-2-pyrrolidone (NMP) is a versatile water-miscib

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

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

13 s were selected based on their solubility in N-methyl-2-pyrrolidone and relevance as a combination th

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

15 bserved that 3-(3'4',5'-trimethoxyphenyl)-5-(N-methyl-3'-indolyl)-1,2,4-triazole compound (also known

16 her the N-methylbenzothiazolium (Btz) or the N-methyl-3,3-dimethylindolium (Ind) acceptors.

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

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

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

20 Modification of their backbone with N-methyl amides inhibits folding, which directly correla

21 process is versatile and can afford valuable N-methyl amino acids and N, O-acetals.

22 Conformational analysis of selected N-methyl analogs indicated the importance of specific am

23 Compared to their N-methyl analogues, N-trifluoromethyl azoles have a high

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

25 gnizes putative metabolites of NADH, such as N-methyl- and N-ribosyl-dihydronicotinamide.

26 By contrast, we did not observe N-methyl arginyl N-demethylation with purified JMJD6.

27 gnment as a lysyl hydroxylase rather than an N-methyl arginyl-demethylase.

28 tivity was achieved mostly by introducing d- N-methyl-Asp instead of Asp at the penultimate position

29 [[(3-iodophenyl)methyl]amino]-9H-purin-9-yl]-N-methyl-beta-d-ribofuranuronamide (IB-MECA).

30 e-step reaction, with the derivatising agent N-methyl-bis-trifluoroacetamide, to substitute the excha

31 ne, there were significantly lower levels of N-methyl carbamates and neonicotinoids in 2011.

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

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

34 We previously showed that N Methyl D Aspartate Receptor (NMDARs), expressed on cer

35 Here we demonstrate that the N-methyl D-aspartate (NMDA) antagonist ketamine is able

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

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

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

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

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

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

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

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

44 N-methyl d-aspartate receptors are ligand-gated ionotrop

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

46 nsmitter glutamate, along with the compounds N-methyl-d-aspartate (NMDA) and d-(-)-2-amino-5-phosphon

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

48 ial agonist of the glycine co-agonist of the N-methyl-D-aspartate (NMDA) glutamate receptor, is poten

49 widely assumed to be mediated by blockade of N-methyl-D-aspartate (NMDA) glutamate receptors, our exp

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

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

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

55 e 1950's until the discovery of ketamine, an N-methyl-D-aspartate (NMDA) receptor antagonist that pro

56 Ketamine, an N-methyl-d-aspartate (NMDA) receptor antagonist, can rap

57 Animal model data suggest that N-methyl-D-aspartate (NMDA) receptor antagonists may blo

58 ntidepressant response to ketamine and other N-methyl-D-aspartate (NMDA) receptor antagonists.

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

60 lice cultures, which could be reversed by an N-methyl-D-aspartate (NMDA) receptor blocker.

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

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

63 N-methyl-D-aspartate (NMDA) receptor-dependent LTP requi

64 a rapid release of H(2) O(2) resulting from N-methyl-D-aspartate (NMDA) receptor-mediated activation

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

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

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

68 N-Methyl-d-aspartate (NMDA) receptors are Ca(2+)-permeab

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

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

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

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

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

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

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

76 in excitatory neurotransmission mediated by n-methyl-d-aspartate (NMDA) receptors following stimulat

77 Context-dependent inhibition of N-methyl-D-aspartate (NMDA) receptors has important ther

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

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

80 N-methyl-D-aspartate (NMDA) receptors mediate synaptic e

81 ther CNS neurotransmitter receptors, such as N-methyl-d-aspartate (NMDA) receptors, affect whole cell

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

83 spine-like structures, and elevated synaptic N-methyl-d-aspartate (NMDA) receptors, thereby increasin

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

85 ing probe that targets the GluN2B subunit of N-methyl-d-aspartate (NMDA) receptors.

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

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

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

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

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

91 microinjection of the glutamatergic agonist N-methyl-d-aspartate (NMDA).

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

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

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

95 -hydroxy-5-methyl-4-isoxazole propionic acid/N-methyl-D-aspartate glutamate currents.

96 -hydroxy-5-methyl-4-isoxazole propionic acid/N-methyl-D-aspartate glutamate ratio and spine head diam

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

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

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

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

101 d-(-)-2-amino-5-phosphonopentanoic acid, or N-methyl-d-aspartate modulation of native or recombinant

102 Over the past decade, various N-methyl-D-aspartate modulators have failed in clinical

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

104 ced by two mechanisms-induced emigration via N-methyl-D-aspartate receptor (NMDA) dependence and rest

105 t mechanism is predominantly mediated by the N-methyl-d-aspartate receptor (NMDA) receptor, although

106 cell-signaling events were dependent on the N-methyl-d-aspartate receptor (NMDA-R) and low-density l

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

108 Increased synaptic N-methyl-d-aspartate receptor (NMDAR) activity in the hy

109 induced potentiation occurred independent of N-methyl-D-aspartate receptor (NMDAR) activity, was acco

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

111 tic function and plasticity by modulation of N-methyl-d-aspartate receptor (NMDAR) and alpha-amino-3-

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

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

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

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

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

117 vailing disinhibition hypothesis posits that N-methyl-d-aspartate receptor (NMDAR) antagonists such a

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

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

120 (ABs) against the NR1 (GluN1) subunit of the N-methyl-d-aspartate receptor (NMDAR) are among the most

121 ed cytoskeleton-associated protein (ARC) and N-methyl-D-aspartate receptor (NMDAR) complexes; however

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

123 rate that antibodies from patients with anti-N-methyl-d-aspartate receptor (NMDAR) encephalitis alter

124 Anti-N-methyl-d-aspartate receptor (NMDAR) encephalitis is an

125 Anti-N-methyl-D-aspartate receptor (NMDAR) encephalitis is th

126 most common cause of autoimmune catatonia is N-methyl-D-aspartate receptor (NMDAR) encephalitis, whic

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

128 Of these, the N-methyl-d-aspartate receptor (NMDAR) family has many cr

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

130 ug of 7-chlorokynurenic acid (7-Cl-KYNA), an N-methyl-D-aspartate receptor (NMDAR) glycine site antag

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

132 underlying this is unclear but may be due to N-methyl-D-aspartate receptor (NMDAR) hypofunction and p

133 N-methyl-D-aspartate receptor (NMDAR) hypofunction has b

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

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

136 The N-methyl-d-aspartate receptor (NMDAR) is an ion channel

137 gates the potentiation of excitatory GluN2B N-methyl-d-aspartate receptor (NMDAR) responses at lamin

138 Downward FRH did not require N-methyl-D-aspartate receptor (NMDAR) signaling and was

139 Alterations of the N-methyl-d-aspartate receptor (NMDAR) subunit GluN2A, en

140 We demonstrate that the developmental N-methyl-D-aspartate receptor (NMDAR) subunit switch fro

141 the methionine cycle, is a known agonist of N-methyl-d-aspartate receptor (NMDAR), a glutamate recep

142 imaging agent for the GluN2B subunits of the N-methyl-d-aspartate receptor (NMDAR), a key therapeutic

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

144 istration improves outcomes in patients with N-methyl-D-aspartate receptor (NMDAR)-antibody encephali

145 All three compounds reduced N-methyl-D-aspartate receptor (NMDAR)-mediated currents

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

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

148 s, autoimmune neuroinflammation (due to anti-N-methyl-D-aspartate receptor [NMDA] encephalitis and mu

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

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

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

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

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

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

155 sthetic doses of ketamine, a non-competitive N-methyl-D-aspartate receptor antagonist(2,3), provide r

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

157 rts the rapid antidepressant efficacy of the N-methyl-D-aspartate receptor antagonist, ketamine, for

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

159 -like effects of ketamine, a non-competitive N-methyl-D-aspartate receptor antagonist, which produces

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

161 169 (49%) patients and measurements of anti-N-methyl-D-aspartate receptor antibodies were taken in 4

162 ive for neuronal autoantibodies (principally N-methyl-D-aspartate receptor antibodies) and who have r

163 blind, placebo-controlled clinical trials of N-methyl-D-aspartate receptor augmentation of psychotrop

164 bly resulting in reduced availability of the N-methyl-D-aspartate receptor coagonists glycine and D-s

165 disseminated encephalomyelitis, and 6% anti-N-methyl-d-aspartate receptor encephalitis; and 17% (95%

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

167 alities are also present in a mouse model of N-methyl-D-aspartate receptor hypofunction (Ppp1r2cre/Gr

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

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

170 xcitatory postsynaptic current frequency and N-methyl-D-aspartate receptor hypofunction.

171 receptor coagonists glycine and D-serine and N-methyl-D-aspartate receptor hypofunction.

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

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

174 o reverse such deficits in humans, including N-methyl-D-aspartate receptor modulators (ketamine, D-cy

175 as reduced substantially upon addition of an N-methyl-D-aspartate receptor peptide analog but not ATP

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

179 diated specifically successive impairment of N-methyl-d-aspartate receptor subunit 2B (NR2B), postsyn

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

181 val may be related to an upregulation of the N-methyl-D-aspartate receptor subunits NR1 and NR2A.

182 ates for imaging the NR2B subunit within the N-methyl-d-aspartate receptor with PET.

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

184 ephrine mediated nociception modulation, and N-methyl-D-aspartate receptor, NMDAR, antagonism.

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

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

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

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

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

190 probe for imaging the GluN2B subunits of the N-methyl-d-aspartate receptor.

191 3A1, are tightly controlled by activation of N-methyl-D-aspartate receptors (NMDAR) containing the Gl

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

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

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

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

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

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

198 N-methyl-D-aspartate receptors (NMDARs) are required to

199 cal arteriole lumen diameter is regulated by N-methyl-d-aspartate receptors (NMDARs) expressed by bra

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

201 Antibodies against neuronal N-methyl-D-aspartate receptors (NMDARs) in patients with

202 n meditated by glutamate receptors including N-methyl-D-aspartate receptors (NMDARs) is pivotal to br

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

204 N-Methyl-D-aspartate receptors (NMDARs) play critical ro

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

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

207 ith improved characteristics for imaging the N-methyl-d-aspartate receptors (NMDARs) subtype 2B (GluN

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

209 wed no antibodies against natively expressed N-methyl-D-aspartate receptors (NMDARs), or the surface

210 involving activation by glutamate ligands of N-methyl-D-aspartate receptors (NMDARs), which is key in

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

212 e investigated the properties of presynaptic N-methyl-d-aspartate receptors (pre-NMDARs) at corticohi

213 roinflammation as well as restored levels of N-methyl-d-aspartate receptors and post-synaptic markers

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

215 d that this effect requires open presynaptic N-methyl-d-aspartate receptors but not plasmin generatio

216 strocytic calcium signaling, and presynaptic N-methyl-D-aspartate receptors coupled with calcineurin

217 elective inhibitors of the GluN2B subunit of N-methyl-d-aspartate receptors in the ionotropic glutama

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

219 cid receptors, and GluN2B-subunit containing N-methyl-D-aspartate receptors, but not GluA1 subunit co

220 ) inputs, abGCs directly excite mGCs through N-methyl-d-aspartate receptors.

221 1,4,5-trisphosphate receptor as well as the N-methyl-d-aspartate receptors.

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

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

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

225 h as the non-receptor tyrosine kinase Src or N-methyl-D-aspartate receptors.

226 Localization of the N-methyl-D-aspartate type glutamate receptor (NMDAR) to

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

228 N-Methyl-d-aspartate type glutamate receptors (NMDARs) a

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

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

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

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

233 NU-120596 and NS-1738 on the spontaneous and N-methyl-D-aspartate-evoked (NMDA-evoked) firing rate of

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

235 CSF from patients with either N-methyl-D-aspartate-receptor-antibody (pCSF(NMDAR), n =

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

237 Similarly, USP6 expression regulates N-methyl-D-aspartate-type glutamate receptor (NMDAR)-dep

238 Contributions of N-methyl-D-aspartate-type glutamate receptors (NMDARs) t

239 henyl-butyl-tert-nitrone (alphaPBN), and the N-methyl-D-aspartic acid (NMDA) antagonist MK801-in mous

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

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

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

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

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

245 ate and glycine agonist-binding sites of the N-methyl-d-aspartic acid receptor.

246 tory synapses by interacting and trafficking N-methyl-D-aspartic acid receptors (NMDAR) and alpha-ami

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

248 Appending N-methyl-d-glucamine (NMDG) to the pore walls of high-su

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

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

251 eticulum Ca release, while QX-flecainide and N-methyl flecainide did not.

252 r tachyarrhythmias in Casq2-/- mice, whereas N-methyl flecainide had no significant effect on arrhyth

253 ated flecainide analogues (QX-flecainide and N-methyl flecainide) and showed that N-methylation reduc

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

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

256 of 9 metabolites, including phenethylamine, N-methyl-glutamate, and agmatine (P < 0.05).

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

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

259 yl with an ethyl group or adding a second 1'-N-methyl group significantly reduced interaction with al

260 ence of a base in HFIP, whereas pyrroles and N-methyl indoles undergo cyclization in the presence of

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

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

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

264 contacts the lithium-metal anode and a poly(N-methyl-malonic amide) contacts the cathode.

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

266 d cell lines exposed to the alkylating agent N-methyl-N'-nitro-N-nitrosoguanidine (MNNG).

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

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

269 1-(2-chlorophenyl)-N-methyl-N-(1-methylpropyl)-3-isoquinolinecarboxamide (P

270 nding, the N-methylated analog, 2,5-dichloro-N-methyl-N-(2-methyl-4-nitrophenyl)benzenesulfonamide (F

271 st, the radical cation derived from 4-chloro-N-methyl-N-(2-phenylcyclopropyl)aniline (8) undergoes cy

272 n of the fluorescence probe 6-dodecanoyl-2-[ N-methyl-N-(carboxymethyl)amino] naphthalene, a sensor f

273 e obtained with 10 uM 2-(3,4-dichlorophenyl)-N-methyl-N-[(1R,2R)-2-pyrrolidin-1-ylcyclohexyl]acetamid

274 ght method has been used for deprotection of N-methyl-N-arylsulfonamides with Hantzsch ester (HE) ani

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

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

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

278 (Citrus sinensis) after derivatization with N-methyl-N-trimethylsilyltrifluoroacetamide using a targ

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

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

281 anes stabilized by ortho-benzamide (oBA) and N-methyl ortho-benzamide (MoBA) ligands have been synthe

282 Nevertheless, the UV-Vis spectra of N-methyl-oxybenzi- and N-methyl-oxypyriporphyrins were d

283 N-Methyl-oxybenzi- and N-methyltropiporphyrins reacted w

284 the UV-Vis spectra of N-methyl-oxybenzi- and N-methyl-oxypyriporphyrins were dramatically altered and

285 N-methyl perfluorobutane sulfonamidoacetic acid (MeFBSAA

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

287 e a possible mechanism for the production of N-methyl proline by the gut microbiome.

288 limosum ATCC 8486, an acetogen that excretes N-methyl proline during growth on proline betaine, we de

289 intravitreal injection of the FECH inhibitor N-methyl protoporphyrin had similar effects.

290 2-pyrimidine, vinyl-2-pyridine, and vinyl-2-(N-methyl)-pyridine groups conferred reversible, time-dep

291 ed using encoded library technology, with an N-methyl pyridone series identified through fragment scr

292 the amido-like structures of the N-confused N-methyl pyrrole rings of the macrocycles.

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

294 rties, and the proton NMR spectra showed the N-methyl resonances near -3 ppm.

295 ate the ribosomal formation of thioamide and N-methyl-thioamide bonds in linear as well as macrocycli

296 on of adrenaline-synthesizing enzyme, phenyl-N-methyl transferase, by adrenal chromaffin cells and ch

297 x-membered heteroaryl groups in place of the N-methyl triazolyl moiety in 6.

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 Replacing the 1'-N-methyl with an ethyl group or adding a second 1'-N-met