ライフサイエンスコーパス: tetraethylammonium

1 el function with permeability to K+ > Na+ >> tetraethylammonium.

2 expressing cells is insensitive to 25 mmol/L tetraethylammonium.

3 illations, as they are completely blocked by tetraethylammonium.

4 enaline, 50 microM 2-chloroadenosine or 5 mM tetraethylammonium.

5 s partially sensitive to 4-aminopyridine and tetraethylammonium.

6 in, 3,4-diaminopyridine, 4-aminopyridine and tetraethylammonium.

7 ter tension when K+ channels were blocked by tetraethylammonium.

8 sulfonate and alter reversible inhibition by tetraethylammonium.

9 sensitive to the potassium channel inhibitor tetraethylammonium.

10 ficantly lower than a LOD of less lipophilic tetraethylammonium.

11 ions but did not affect plateaus unmasked by tetraethylammonium.

12 otic frequency evoked by bath application of tetraethylammonium (1-10 mM) was significantly enhanced

13 y of SjAQP was inhibited by 1 mM HgCl2, 3 mM tetraethylammonium, 1 mM ZnCl2, and 1 mM CuSO4.

14 Tetraethylammonium 10(-3) mol/L but not glibenclamide 10

15 ntrast, the non-specific K+ channel blockers tetraethylammonium (10 mM) and 4-aminopyridine (10 mM) m

16 The SOR and RD were blocked by external tetraethylammonium (10 mM) and Ba2+ (0.1-0.5 mM).

17 The K+ channel blocker tetraethylammonium (10 mM) generated inward currents sim

18 (5 mM), tetrapentylammonium (10 microM) and tetraethylammonium (10 mM).

19 TRESK-2 was insensitive to 1 mm tetraethylammonium, 100 nm apamin, 1 mm 4-aminopyridine,

20 To assess Oct1 function, the model substrate tetraethylammonium ([(14)C]TEA) was administered intrave

21 ptake of the quaternary organic cation [14C]-tetraethylammonium ([14C]-TEA), with a Km of 38 micromol

22 ne (15% inhibition) and insensitive to 10 mM tetraethylammonium, 2 mM Ca2+, 1 mM Cd2+ and 50 microM L

23 was inhibited by 4-aminopyridine (10 mM) and tetraethylammonium (4-25 mM), but insensitive to charybd

24 f the potassium delayed rectifier current by tetraethylammonium (5 mM) or the hyperpolarization-activ

25 t density and currents that are inhibited by tetraethylammonium (5 mmol/L) or charybdotoxin (100 nmol

26 Tetraethylammonium, a pore blocker, did not affect the r

27 h variants abolished OCT1-mediated uptake of tetraethylammonium, a typical OCT1 substrate, and were n

28 imulated by flufenamic acid and inhibited by tetraethylammonium; a voltage-gated inward Na+ current;

29 ive to 4-aminopyridine but is insensitive to tetraethylammonium, alpha-dendrotoxin, and E-4031.

30 e widely used Kv channel blockers, including tetraethylammonium, alpha-dendrotoxin, phrixotoxin-2, an

31 Treatment with 500 microM tetraethylammonium also decreased the latency to AP gene

32 The K+ channel blocker tetraethylammonium also inhibited oligodendrocyte progen

33 cate that neither 4-aminopyridine (4-AP) nor tetraethylammonium alters normal nerve conduction.

34 In contrast, 1.5 mM tetraethylammonium, an organic cation, blocked uptake of

35 the rate of transport of the fixed cations, tetraethylammonium and 1-methyl-4-phenylpyridinium, i.e.

36 d-spectrum of K+ channel blockers, including tetraethylammonium and 4-aminopyridine, and insensitive

37 Unexpectedly, also the organic cations Tetraethylammonium and Acetylcholine were transported in

38 the nonselective potassium channel blockers tetraethylammonium and barium.

39 nels were Ca2+-dependent and were blocked by tetraethylammonium and charybdotoxin in normal and infla

40 eLa cells, the cDNA induces the transport of tetraethylammonium and guanidine.

41 f this particular mutation on the binding of tetraethylammonium and hydroxylamine, support the hypoth

42 Inhibition by tetraethylammonium and iberiotoxin suggested that these

43 Tetraethylammonium and iberiotoxin, preferential KCa-cha

44 ubthreshold voltages was unaffected by 10 mM tetraethylammonium and likely represents I(A), because i

45 retic uptake of K+ and other cations such as tetraethylammonium and lysine by rat liver mitochondria

46 and Cs+, but the organic monovalent cations tetraethylammonium and N-methyl-D-glucamine are much les

47 oth small monovalent organic cations such as tetraethylammonium and N1-methylnicotinamide and bulkier

48 a calcium spike elicited in the presence of tetraethylammonium and tetrodotoxin.

49 omponent of K+ current sensitive to quinine, tetraethylammonium, and 4-aminopyridine, with IC50 value

50 lso increased fluorescence, whereas choline, tetraethylammonium, and N-methyl-D-glucamine did not.

51 Quaternary amines (tetramethylammonium, tetraethylammonium, and tetrapropylammonium, TMA, TEA, a

52 large pore as inferred from permeability to tetraethylammonium (approximately 8.5 angstroms diameter

53 ntally with a calcium selective membrane and tetraethylammonium as a model interfering agent, and the

54 halide ions in an aqueous sample containing tetraethylammonium benzoate, (b) capture of the released

55 Internal application of tetraethylammonium blocked BK channel activity in a mann

56 oncentration of permeant ions, we argue that tetraethylammonium blocks by occluding the external end

57 In contrast, simulations indicate that tetraethylammonium blocks movement of metal cations.

58 ative measurements of atenolol, tioconazole, tetraethylammonium bromide, and tetrabutylammonium iodid

59 For the tetraethylammonium bromide/carbon tetrabromide dyad, the

60 to alpha-dendrotoxin, paxilline, apamin, and tetraethylammonium but sensitive to 4-aminopyridine and

61 e insensitive to 20 microM verapamil or 1 mM tetraethylammonium, but inhibited by 0.5 mM Ba(2+) or 0.

62 rganic anions, but not by the organic cation tetraethylammonium, by the multidrug resistance ATPase i

63 d in a near-homogeneous system that utilizes tetraethylammonium carbonate as base, 8-hydroxyquinoline

64 The tetraethylammonium carceplex, 1b, has been characterized

65 these states may be controlled by using the tetraethylammonium cation (TEA(+)) and/or iodide anion (

66 storage times in UW solution as assessed by tetraethylammonium cation transport (TEA).

67 In contrast, the addition of a tetraethylammonium cation, which binds more effectively

68 ut affecting the affinity of the channel for tetraethylammonium, charybdotoxin, and nifedipine.

69 ofilium and 4-aminopyridine and partially by tetraethylammonium, charybdotoxin, dendrotoxin, and kali

70 e inhibition was not blocked by low doses of tetraethylammonium chloride (1 mM), barium, or glibencla

71 acellular electrodes in solutions containing tetraethylammonium chloride (10 mM) and BaCl2, (1 mM).

72 mide (10 microM), 4-aminopyridine (3 mM) and tetraethylammonium chloride (10 mM) did not affect L-lac

73 ith 4-aminopyridine (5 mM) but unaffected by tetraethylammonium chloride (20 mM) or blockers of Na(+)

74 ly blocked by 4-aminopyridine (4 mM) but not tetraethylammonium chloride (30 mM) and did not show ina

75 ing various concentrations of the ionic salt tetraethylammonium chloride (TEA(+)Cl(-)) or the zwitter

76 ns could be induced easily by Bay K8644 plus tetraethylammonium chloride (TEA) or [TEA]o after Cs+ re

77 Tetraethylammonium chloride (TEA) was used to inhibit K(

78 nnel blockers, including chlorotoxin (Ctx),, tetraethylammonium chloride (TEA), and tamoxifen.

79 lamp in the presence of 15 mM CsCl and 15 mM tetraethylammonium chloride (TEA-Cl) to eliminate K+ cha

80 waves and phasic contractions stimulated by tetraethylammonium chloride (TEA; 10 mM), but did not si

81 were separated in 100% methanol with 12.5 mM tetraethylammonium chloride added as a charge carrier.

82 outward and inward components, prevented by tetraethylammonium chloride and tetrodotoxin, respective

83 not affected at 10(-2) M; on the other hand, tetraethylammonium chloride failed to inhibit either che

84 f MIN6 cells with glucose in the presence of tetraethylammonium chloride generated concomitant Ca2+ a

85 ibition of K+ channels with charybdotoxin or tetraethylammonium chloride produced a modest transient

86 The effects of lidocaine were not blocked by tetraethylammonium chloride, 4-aminopyridine, glibenclam

87 ed potassium channels (blocked by 250 microM tetraethylammonium chloride, 70 nM charybdotoxin, or 100

88 and econazole, and the K+ channel blockers, tetraethylammonium chloride, apamin, and charybdotoxin,

89 amine-containing compounds tetramethyl- and tetraethylammonium chloride, glutamine, and urea.

90 application of potassium channel antagonist tetraethylammonium chloride, iberiotoxin, or 4-aminopyri

91 annels were already blocked by submillimolar tetraethylammonium chloride, indicating that Cav2.1 (Q-t

92 arbor depended upon voltage-gated sodium and tetraethylammonium chloride-sensitive potassium channels

93 tidine or with the potassium channel blocker tetraethylammonium chloride.

94 e channel blockers glyburide, gadolinium, or tetraethylammonium-Cl did not alter hypotonic-induced sw

95 (+), and Rb(+) and was not inhibited by high tetraethylammonium concentrations.

96 inhibited by K+ channel blockers, including tetraethylammonium, Cs+, and Ba2+.

97 of CMECs was blocked to a similar extent by tetraethylammonium, currents in the stretched endothelia

98 by MPP+ (1-methyl-4-phenylpyridinium), TEA (tetraethylammonium), decynium-22, carnitine, PHA (p-amin

99 ium to the inactivated channel, although the tetraethylammonium does not interact directly with the K

100 Under voltage clamp conditions, tetraethylammonium evokes inward currents that are conce

101 Demetalation with tetraethylammonium fluoride quantitatively generates the

102 hat which determines sensitivity to external tetraethylammonium for voltage-gated potassium channels

103 Tetraethylammonium, glibenclamide, and a high concentrat

104 T transports classic OCT substrates, such as tetraethylammonium, guanidine, and histamine.

105 epolarized conditioning blocked the TOC, but tetraethylammonium had no effect.

106 nents were both blocked potently by external tetraethylammonium (half-block by 150 microm) and 4-amin

107 IK2 were sensitive to high concentrations of tetraethylammonium (half-maximal block at approximately

108 spinal fluid (ACSF), 5 mM Cs+ in ACSF, 20 mM tetraethylammonium in ACSF, or 1 mM 4-aminopyridine in A

109 l and attenuated by glibenclamide as well as tetraethylammonium, in agreement with established respon

110 heir ability to transport the organic cation tetraethylammonium indicating that their effect on carni

111 minopyridine, Ca2+ (10(-8) to 10(-6) M), and tetraethylammonium (internal or external) were without e

112 s are more sensitive to blockade by internal tetraethylammonium ion (TEA) than KvLQT1 channels.

113 Unlike the tetraethylammonium ion (TEA), neither JC638.2alpha nor C

114 We propose that 4AP, like tetraethylammonium ion and other quaternary ammonium ion

115 The tetraethylammonium ion fits snugly in the interior of th

116 ly with KCNQ5 by patch clamp analysis of the tetraethylammonium ion sensitivity of the resulting curr

117 ansport down its diffusion gradient, whereas tetraethylammonium ion substitution for K+ did not affec

118 with a molecule (diethyl ether) or a cation (tetraethylammonium ion) trapped inside.

119 potentiation occurred in the presence of the tetraethylammonium ion, a K+-channel blocker.

120 In the first, we constructed a mutant tetraethylammonium ion-sensitive KCNQ4 subunit and teste

121 y, at very low and at high concentrations of tetraethylammonium ion.

122 +10 mV, indicating increased permeability of tetraethylammonium ion.

123 was confirmed by studying simple transfer of tetraethylammonium ion.

124 er currents by using the BK channel blockers tetraethylammonium ions (TEA(+); 1 mM) or iberiotoxin (2

125 e silent arteries by charybdotoxin (CTX) and tetraethylammonium ions (TEA) induced dose-dependent dep

126 ns, the K+ channel blockers 4-aminopyridine, tetraethylammonium ions and XE991.

127 ation was perturbed by application of either tetraethylammonium ions or the Shaker (Sh)B peptide to t

128 efflux is approximately 0.1 mM), but not by tetraethylammonium ions or verapamil.

129 The IK(V) was blocked by tetraethylammonium ions with an IC50 of 5.2 mM and was u

130 inopyridine and quinine and insensitivity to tetraethylammonium ions.

131 nt cations including tetramethylammonium and tetraethylammonium ions.

132 Since inhibition by external tetraethylammonium is sensitive to voltage and to the in

133 nd stichodactylatoxin, and is insensitive to tetraethylammonium, kaliotoxin, and charybdotoxin.

134 urrent that is blocked by externally applied tetraethylammonium (Kd = 30 +/- 7 mM), charybdotoxin (Kd

135 thiosulfonate ethylammonium (MTSEA) and MTS tetraethylammonium (MTSET) was tested.

136 ost of the Cl- with largely impermeant ions (tetraethylammonium, N-methyl-D-glucamine and methanesulp

137 s (Ik) were small and were inhibited by 1 mM tetraethylammonium or 100 nM charybdotoxin (CTX; a speci

138 Exchanging the sodium cation with tetraethylammonium or didodecyldimethylammonium expands

139 Attenuating outward K+ current with tetraethylammonium or elevated extracellular K+, but not

140 K(+) currents were suppressed by tetraethylammonium or N-methylglucamine in the solutions

141 iation (LTP) induced either chemically (with tetraethylammonium), or by high-frequency (200-Hz) elect

142 y extracellular tetrodotoxin, nimodipine, or tetraethylammonium, or by intracellular dialysis with 4-

143 on exchange with either tetramethylammonium, tetraethylammonium, or tetrabutylammonium cations to yie

144 nsensitivity to all other inhibitors tested (tetraethylammonium, quinine, Cs(+), tetrodotoxin, verapa

145 In addition, 0.5 mM tetraethylammonium reduced I(M), suggesting that I(M) wa

146 The IK blocker tetraethylammonium reversed the ischemia-induced suppres

147 xceeding 10(14) M(-1) have been measured for tetraethylammonium salts in chloroform by employing a va

148 sted for binding to seven monovalent anions (tetraethylammonium salts, wet chloroform as solvent).

149 components of the whole-cell current were a tetraethylammonium-sensitive (IC50 = 9 mM), iberiotoxin-

150 hat CrMP decreases the open probability of a tetraethylammonium-sensitive (TEA-sensitive) 105 pS K ch

151 eous vasodilatation is mediated, in part, by tetraethylammonium-sensitive calcium-dependent potassium

152 units underlie the more slowly inactivating, tetraethylammonium-sensitive component of I(K, slow).

153 s absent (n=6), the density of the 20-mmol/L tetraethylammonium-sensitive component of I(K,slow) was

154 VLM- and PVN-projecting neurons had similar, tetraethylammonium-sensitive IK.

155 The ensuing decrease in tetraethylammonium-sensitive K(+) current activation slo

156 Onset cells have a unique high-threshold tetraethylammonium-sensitive K(+) current.

157 ional tetrodotoxin (TTX)-sensitive Na(+) and tetraethylammonium-sensitive K(+) currents.

158 In somatic membrane patches, we observed tetraethylammonium-sensitive K(DR) currents that activat

159 of different ratios of 4-aminopyridine- and tetraethylammonium-sensitive K+ currents.

160 In many nigral neurons, I(CAN) is masked by tetraethylammonium-sensitive potassium conductances, but

161 Tetraethylammonium-sensitive voltage-gated fibroblast cu

162 ) differed from ventricular muscle in having tetraethylammonium sensitivity and slower recovery.

163 as DPP6 knockdown reduced, I(to) density and tetraethylammonium sensitivity in canine PF but not in v

164 on and inactivation parameters, and external tetraethylammonium sensitivity were all similar to those

165 annels endows SK channels with an equivalent tetraethylammonium sensitivity, indicating that the oute

166 d tetraethylammonium, with Tyr185 conferring tetraethylammonium sensitivity.

167 hift in the concentration-response curve for tetraethylammonium; similar results were evident with ib

168 vated potassium channels by charybdotoxin or tetraethylammonium slowed the repolarizing phase of the

169 rmation of the occluded, economical template tetraethylammonium (TEA(+) ) has been systematically exa

170 lipid bilayers reduced the effectiveness of tetraethylammonium (TEA(+)) as a blocker of K(+) translo

171 tigate the kinetics of the rapid transfer of tetraethylammonium (TEA(+)) at the 1,2-dichloroethane/wa

172 K(+) currents, which were inhibited by 5 mM tetraethylammonium (TEA(+)) chloride.

173 en Li(+) was the countercation compared with tetraethylammonium (TEA(+)), due to the coordination of

174 TP), LTP induced by the K(+) channel blocker tetraethylammonium (TEA) (TEA-LTP), and mossy fiber (MF)

175 Replacing external Na+ with tetraethylammonium (TEA) abolished the decrease in Gm.

176 epolarizations, and could be blocked by both tetraethylammonium (TEA) and 4-aminopyridine (4-AP).

177 sion with the potassium channel antagonists, tetraethylammonium (TEA) and 4-aminopyridine (4-AP).

178 f delayed rectifier K+ currents inhibited by tetraethylammonium (TEA) and 4-aminopyridine, with simil

179 sitive to block by external charybdotoxin or tetraethylammonium (TEA) and by internal Ba2+.

180 in the presence of the external pore blocker tetraethylammonium (TEA) and depended on a residue requi

181 lity and spike broadening in the presence of tetraethylammonium (TEA) and nifedipine.

182 ult-type nicotinic acetylcholine receptor by tetraethylammonium (TEA) and related quaternary ammonium

183 sistent with this possibility, extracellular tetraethylammonium (TEA) and tetramethylammonium applica

184 ely 11 msec) current insensitive to block by tetraethylammonium (TEA) and variably blocked by 4-amino

185 The location of the tetraethylammonium (TEA) binding site in the outer vesti

186 a mixed alkali metal reaction gel containing tetraethylammonium (TEA) cations.

187 ice, the addition of apamin with glucose and tetraethylammonium (TEA) caused a similar elevation in [

188 ained outward current that can be blocked by tetraethylammonium (TEA) characteristic of a delayed rec

189 Here we show that the nonmercurial compound, tetraethylammonium (TEA) chloride, reduces the water per

190 The K+ channel inhibitors Ba2+, Cs+, and tetraethylammonium (TEA) had distinct effects on differe

191 The uptake of [14C]tetraethylammonium (TEA) in oocytes injected with the cR

192 ions of 4-AP (1 mM) in combination with 5 mM tetraethylammonium (TEA) induce spontaneous synchronized

193 veratridine or blockage of K+ channels with tetraethylammonium (TEA) inhibit oligodendrocyte progeni

194 Intracellular tetraethylammonium (TEA) inhibition was studied at the s

195 Changes in the chemical structure of the tetraethylammonium (TEA) ion reduce binding affinity at

196 Tetraethylammonium (TEA) is frequently used to inhibit d

197 ected by 0.5 mM 4-aminopyridine (4-AP), 1 mM tetraethylammonium (TEA) or 1-10 nM margatoxin.

198 Exposure to the inhibitors of IK, tetraethylammonium (TEA) or 4-aminopyridine (4-AP), redu

199 annel blocker 4-aminopyridine (4-AP) but not tetraethylammonium (TEA) or dendrotoxin (DTX).

200 We show here that tetraethylammonium (TEA) plus 4-aminopyridine (4-AP) whi

201 -40 mV was slowly activating, long-lasting, tetraethylammonium (TEA) sensitive and showed little ste

202 GluR agonists and the K+ channel blocker tetraethylammonium (TEA) strongly inhibited delayed rect

203 Tetraethylammonium (TEA) transport also was investigated

204 The prototype for organic cations tetraethylammonium (TEA) was also transported by SlCAT2.

205 tive muscarinic potassium channels (KACh) by tetraethylammonium (TEA) was studied at 35 degrees C in

206 Internal Cs+ and external tetraethylammonium (TEA) were used to suppress outward c

207 imilar selectivity for some substrates (e.g. tetraethylammonium (TEA)), they have distinct selectivit

208 MLA, applied topically to skin surface), (2) tetraethylammonium (TEA), (3) EMLA + TEA (Combo), and (4

209 ), a non-specific NOS inhibitor; (iii) 50 mm tetraethylammonium (TEA), a non-specific KCa channel blo

210 e of the membrane (trans-ions), and external tetraethylammonium (TEA), an I(Ks) pore-blocker.

211 ester (l-NAME), (3) a KCa channel inhibitor, tetraethylammonium (TEA), and (4) TEA + l-NAME.

212 A nonselective K(+) channel blocker, tetraethylammonium (TEA), and a large-conductance Ca(2+)

213 , the nonselective potassium channel blocker tetraethylammonium (TEA), and the selective adenosine tr

214 We previously observed that tetraethylammonium (TEA), high extracellular potassium,

215 K+ channel blockers, apamin, d-tubocurarine, tetraethylammonium (TEA), or intracellular Cs+ decreased

216 t using various chloride salts, specifically tetraethylammonium (TEA), tetrapropylammonium (TPA), tet

217 ified in blLPM vesicles, including thiamine, tetraethylammonium (TEA), tri-n-butyl-methylammonium (TB

218 Because all K+ channels are blocked by tetraethylammonium (TEA), we asked if TEA would inhibit

219 ective effects of 4-aminopyridine (4-AP) and tetraethylammonium (TEA), which block the potassium chan

220 ult rat hippocampal slices with BDNF or with tetraethylammonium (TEA), which induces a chemical form

221 They were also inhibited by tetraethylammonium (TEA),an inhibitor of Ca2+-activated

222 ter exocytosis, because it was observed that tetraethylammonium (TEA)-induced inhibition of the delay

223 PMA had no significant effect on the 1 mM tetraethylammonium (TEA)-insensitive outward current or

224 Z: type 1 cells, with 4-aminopyridine (4-AP)/tetraethylammonium (TEA)-sensitive and CdCl(2)-sensitive

225 ow that repolarization is composed of a fast tetraethylammonium (TEA)-sensitive component, determinin

226 extracellular Cs+ (0 K+), there were large, tetraethylammonium (TEA)-sensitive currents.

227 al excitability through inhibition of highly tetraethylammonium (TEA)-sensitive ion channels that con

228 the inward current by approximately 50%, and tetraethylammonium (TEA+) and choline were relatively im

229 Iberiotoxin or 1 mM tetraethylammonium (TEA+) constricted intact arteries.

230 Tetraethylammonium (TEA+) is widely used for reversible

231 channel, unlike native Shaker, to close with tetraethylammonium (TEA+) or the long-chain TEA-derivati

232 Movement of Ca2+, K+, and tetraethylammonium (TEA+) through the model RyR2 pore we

233 a2+ or K+ channel antagonists, verapamil and tetraethylammonium (TEA+).

234 Tetraethylammonium (TEA, 1-10 mM) had little effect on t

235 ng the application of the K+ channel blocker tetraethylammonium (TEA, 10 mM), implicating the involve

236 Tetraethylammonium (TEA; 1 mM) similarly enhanced KCa ex

237 electively blocked by a low concentration of tetraethylammonium (TEA; 1 mM).

238 Tetraethylammonium (TEA; 10 mM), 1 and 5 mM 4-aminopyrid

239 d by Ba2+ (1 mM), 4-aminopyridine (1 mM) and tetraethylammonium (TEA; 20 mM), with an IC50 for TEA of

240 Tetraethylammonium (TEA; 30 mM) reduced the voltage-depe

241 Caesium (100 microM), barium (1 mM), tetraethylammonium (TEA; 5 mM), apamin (10 nM) and 4-ami

242 om) and high concentrations of extracellular tetraethylammonium (TEA; IC(50) = 11.8 mM), but no speci

243 ted K(+) current that is blocked potently by tetraethylammonium (TEA; IC(50), 0.14 mm).

244 We investigated the effect of 1.0 mM tetraethylammonium (TEA; which blocks Kv3 channels) on i

245 riant with changes in [Cl(-)], [Na(+)], and [tetraethylammonium] ([TEA(+)]), but dependent on [H(+)].

246 We found that dimethylamine, triethylamine, tetraethylammonium, tetrabutylammonium, tetrapropylammon

247 bstrate (l-carnitine) and the organic cation tetraethylammonium, three variants showed functional dif

248 potentiated by the binding of extracellular tetraethylammonium to the inactivated channel, although

249 n, even though it allows large ions, such as tetraethylammonium, to permeate readily.

250 In the presence of glucose and tetraethylammonium, transgenically derived beta-cells (b

251 on followed by Western blotting) and reduced tetraethylammonium transport by OCT2 expressed in Chines

252 [(3)H]tetraethylammonium uptake in HeLa cells stably expressin

253 Na(+) (approximately 1.25), insensitivity to tetraethylammonium, voltage independence, and partial se

254 rved in the presence of Bay K 8644, NMDA, or tetraethylammonium were abolished in low-sodium buffer a

255 Low concentrations of tetraethylammonium were used to broaden the presynaptic

256 eation of AgAQP1 is inhibited by HgCl(2) and tetraethylammonium, with Tyr185 conferring tetraethylamm

257 thiolate complexes (Et4N)Ni(X-pyS)3 (Et4N = tetraethylammonium; X = 5-H (1a), 5-Cl (1b), 5-CF3 (1c),