ライフサイエンスコーパス: delayed rectifier

1 neurons is dominated by another unidentified delayed rectifier.

2 In most cells, the dominant Kv current was a delayed rectifier.

3 he SLO-2 current is a major component of the delayed rectifier.

4 eptors target only the fast component of the delayed rectifier.

5 uppress pro-arrhythmic events than the rapid delayed rectifier.

6 hannels (R- and T-type calcium, fast sodium, delayed rectifier, A-type, and small-conductance calcium

7 The delayed rectifier activated at potentials above -20 mV a

8 Extra-subfamily delayed rectifier alpha-subunits, regardless of their ca

9 e N-type alpha-subunits with intra-subfamily delayed rectifier alpha-subunits.

10 nnels comprising both N-type and non-N-type (delayed rectifier) alpha-subunits depends upon the numbe

11 ing enteric neurotransmission or by blocking delayed rectifier and ATP-sensitive K(+) currents.

12 ABA(A) and glycine), ion channels (potassium delayed rectifier and I(h)) and gap junctions.

13 Blockade of delayed rectifiers and A-like K+ channels, by tityustoxi

14 lective loss of circadian modulation of fast delayed-rectifier and A-type K+ currents was observed.

15 currents: the sodium current and the M-type, delayed rectifier, and calcium-dependent potassium curre

16 ron with stochastic ion channels exclude the delayed rectifier as a possible noise source.

17 l activity of the pancreatic islet beta-cell-delayed rectifier channel, Kv2.1.

18 ls, and had smaller outward currents through delayed rectifier channels (I(KV)) and noninactivating c

19 Kv2 delayed rectifier channels are, however, unique exceptio

20 channel can be distinguished from most other delayed rectifier channels by its very high threshold of

21 bundance, knowledge of the function of these delayed rectifier channels has been limited by the lack

22 re capable of forming functional heteromeric delayed rectifier channels.

23 probability, through increased activation of delayed rectifier channels.

24 dicate that Kv2 subunits function as classic delayed-rectifier channels in vertebrate neurons.

25 -subunits, versus their slowly inactivating (delayed rectifier) counterparts.

26 ing channel conductance to generate the slow delayed rectifier current ( I Ks) that is critical for t

27 virus-expressed RFFL exhibited reduced rapid delayed rectifier current (I (Kr)).

28 subunits together mediates the cardiac slow delayed rectifier current (I (Ks) ), which is partly res

29 D) by interacting with Q1 and augmenting the delayed rectifier current (I(K)).

30 ed by coronary microembolizations, the rapid delayed rectifier current (I(Kr)) density was increased.

31 The rapidly delayed rectifier current (I(Kr)) has been described in

32 KCNQ1, which can function either as the slow delayed rectifier current (I(Ks)) of the cardiac action

33 (+) ) currents such as the slowly activating delayed rectifier current (IKs ) and the small conductan

34 e electrophysiological recording of the slow delayed rectifier current (IKs) and investigation of pha

35 larization is determined in part by the slow delayed rectifier current (IKs), through the tetrameric

36 Kv1.5 channels conduct the ultrarapid delayed rectifier current (IKur) that contributes to act

37 of genes encoding the slow component of the delayed rectifier current (LQT1, LQT5), the rapid compon

38 ent (LQT1, LQT5), the rapid component of the delayed rectifier current (LQT2, LQT6), or the Na(+) cur

39 ociated with an increase in the amplitude of delayed rectifier current and a shift of activation towa

40 el subtype might contribute to the beta-cell delayed rectifier current and that this current could be

41 Blockade of the potassium delayed rectifier current by tetraethylammonium (5 mM) o

42 The major subunit of the cardiac delayed rectifier current I(Kr) is encoded by the human

43 te lowering agent ivabradine block the rapid delayed rectifier current I(Kr), prolong action potentia

44 75X mutant failed to generate the ultrarapid delayed rectifier current I(Kur) vital for atrial repola

45 channel that conducts the rapidly activating delayed rectifier current in the heart.

46 malian brain and is a major component of the delayed rectifier current in the hippocampus.

47 in murine portal vein and contribute to the delayed rectifier current in these myocytes.

48 for the gating of the slow component of the delayed rectifier current is formulated and validated ag

49 parallel with increases in I(Kv) and produce delayed rectifier current when heterologously expressed,

50 Both cell types expressed a delayed rectifier current with similar voltage dependenc

51 ient outward current, rapid component of the delayed rectifier current, and the L-type calcium curren

52 KCNQ1-KCNE1 channels generate the slow delayed rectifier current, I(Ks), which contributes to t

53 gated potassium channels responsible for the delayed rectifier current, including Kv2.1, are usually

54 Namely I(ks), the slowly activating delayed rectifier current, is produced by KvLQT1/KCNE1,

55 (Ks), the slowly activating component of the delayed rectifier current, plays a major role in repolar

56 increased the rapid component, I(Kr), of the delayed rectifier current, thereby accelerating repolari

57 beta-subunit KCNE1 to generate IKs, the slow delayed rectifier current, which plays a critical role i

58 ifen, ethylbromide tamoxifen did not inhibit delayed rectifier current.

59 s responsible for the rapid component of the delayed rectifier current.

60 s because of reduced activation of the rapid delayed-rectifier current IKr.

61 We also determined that the remaining delayed-rectifier current in cultured myocytes was carri

62 nstituting approximately 60-80% of the total delayed-rectifier current.

63 the voltage-dependent activation of neuronal delayed rectifier currents (IK), leading to enhanced IK

64 neuronal M-currents (IK,M) and cardiac slow delayed rectifier currents (IK,s), respectively.

65 operties commensurate with a contribution to delayed rectifier currents and are expressed in neurones

66 Kcna1(-/-) mice lack Kv1.1-delayed rectifier currents and exhibit severe spontaneou

67 rapid decay and reduced peak conductance of delayed rectifier currents from INS-1 cells and from pri

68 -gated potassium (Kv) channel that generates delayed rectifier currents in mammalian heart and brain.

69 les the magnitude and kinetics of endogenous delayed rectifier currents in PC12 cells and hippocampal

70 Delayed rectifier currents sensitive to 4-AP are importa

71 Delayed rectifier currents were not affected by oestroge

72 Our results suggest that the delayed rectifier currents, which regulate action potent

73 an increase in the inactivation rate of the delayed rectifier currents.

74 A-type K(+) current did not increase but the delayed rectifier doubled in adults compared with nymphs

75 with Kv3.1 or Kv3.2 subunits underlie fast, delayed-rectifier (DR) currents that endow neurons with

76 A-type and delayed-rectifier (DR) potassium currents, two putative

77 matic nucleus (SCN) neurons express the fast delayed rectifier (FDR) potassium current and raise ques

78 paration, we show that the magnitude of fast delayed rectifier (FDR) potassium currents has a diurnal

79 ctance, G(BK) , and a low-voltage-activating delayed rectifier, G(K(LV)) , that activates upon elevat

80 functions as a beta subunit for the cardiac delayed rectifier I(Kr), these results suggest that this

81 The delayed rectifier I(Ks) potassium channel, formed by coa

82 K(+) current, possibly the slowly activating delayed rectifier I(Ks), may account in part for this fo

83 minK (KCNE1) produces the slowly activating delayed rectifier I(ks).

84 activated more than 10-fold faster than the delayed rectifier I(Kv) over the physiological voltage r

85 on the density of the inward (I(K1)) and the delayed rectifier (I(K)) currents are more contradictory

86 of the two molecular components of the rapid delayed rectifier (I(K,r)), HERG and KCNE2, have been li

87 ve suggested that the rapid component of the delayed rectifier (I(Kr)) may contribute importantly to

88 ients created by heterogeneities of the slow-delayed rectifier (I(Ks)) and transient outward (I(to))

89 The slow delayed rectifier (I(KS)) channel is composed of KCNQ1 (

90 K subunit underlie slowly activating cardiac delayed rectifier (I(Ks)) in the heart, whereas two othe

91 the T wave through their effect on the rapid-delayed rectifier, I(Kr).

92 taneous betaAS-mediated increase in the slow delayed rectifier, I(Ks), limits betaAS sensitivity.

93 KCNE1 increased the slow component of the delayed rectifier, I(Ks), without clear phenotypic seque

94 n (the BK-type current IK,f in IHCs, and the delayed rectifier IK,n in both cell types).

95 hearing to form the major part of the mature delayed rectifier, IK,s.

96 may assemble with HERG to modulate the rapid delayed rectifier IKr.

97 assium channels) and that block of the rapid delayed rectifier (IKr ) is the primary mechanism whereb

98 ong-QT syndrome by direct block of the rapid delayed rectifier (IKr) also seem to inhibit PI3K signal

99 KCNQ1 and KCNE1 assemble to form the slow delayed rectifier (IKs) channel critical for shortening

100 Cardiac slow delayed rectifier (IKs) channel is composed of KCNQ1 (po

101 The slow delayed rectifier (IKs) channel is composed of the KCNQ1

102 lization was positively correlated with slow delayed rectifier (IKs) current density; 3) KCNQ1 and ca

103 on gating of the transient outward (Ito) and delayed rectifier (IKslow) components of K(+) current wi

104 ts of the cloned channel sqKv1A compose the "delayed rectifier" in the squid giant axon system, but d

105 clinically relevant prediction that the slow delayed rectifier is better able to stabilize the action

106 a repolarization reserve when IKr, the rapid delayed rectifier, is reduced by disease or drug and can

107 CNA5) underlies the human atrial ultra-rapid delayed rectifier K current (I(Kur)).

108 The rapidly activating delayed rectifier K(+) channel (IKr) is encoded by the h

109 ming alpha-subunit of the rapidly activating delayed rectifier K(+) channel in the heart, which plays

110 gene (hERG1), the pore-forming domain of the delayed rectifier K(+) channel in the heart.

111 roduct forms the pore-forming subunit of the delayed rectifier K(+) channel in the heart.

112 rom HEK293 cells stably transfected with the delayed rectifier K(+) channel Kv2.1, long depolarizatio

113 delaying the activation of slowly activating delayed rectifier K(+) channels (I(Ks)), suggesting impo

114 neurons are also sites where Kv2 (the major delayed rectifier K(+) channels in brain) and other PM a

115 nel gene, we show that this gene encodes the delayed rectifier K(+) channels in Drosophila.

116 demonstrate that Kv1-family (Shaker-related) delayed rectifier K(+) channels in the central medial th

117 apidly (I(Kr)) and slowly (I(Ks)) activating delayed rectifier K(+) channels in the heart.

118 Delayed rectifier K(+) channels may mediate the PYK2 act

119 For delayed rectifier K(+) channels, consideration of the me

120 Sustained-regular cells show mainly delayed rectifier K(+) channels.

121 factors governing this activity, we studied delayed rectifier K(+) conductances in acutely isolated

122 The channels which generate the cardiac slow delayed rectifier K(+) current (I (Ks) ) are composed of

123 d the inward rectifier K(+) current (I(K1)), delayed rectifier K(+) current (I(K)), and transient out

124 ody wall muscles showed a specific effect on delayed rectifier K(+) current (I(K)).

125 Rapid delayed rectifier K(+) current (I(Kr)) and late Na(+) cu

126 tions of PD-307243 on the rapid component of delayed rectifier K(+) current (I(Kr)) in rabbit ventric

127 annel responsible for the rapidly activating delayed rectifier K(+) current (I(Kr)).

128 Addition of slowly activating delayed rectifier K(+) current (I(Ks)) blockade led to f

129 gating kinetics of the slow component of the delayed rectifier K(+) current (I(Ks)) contribute to pos

130 The slow delayed rectifier K(+) current (I(Ks)) is a major determ

131 The cardiac-delayed rectifier K(+) current (I(KS)) is carried by a c

132 e (by 90%) of the atrial-specific ultrarapid delayed rectifier K(+) current (I(Kur)), or the transien

133 Rabbit ventricular rapidly activating delayed rectifier K(+) current (IKr ) amplitude and volt

134 nhanced rabbit ventricular slowly activating delayed rectifier K(+) current (IKs ) by negatively shif

135 ABSTRACT: The slowly activating delayed rectifier K(+) current (IKs ) contributes to rep

136 The atrial-specific ultrarapid delayed rectifier K(+) current (IKur) inactivates slowly

137 ucleated patches showed that GTx inhibited a delayed rectifier K(+) current activating beyond -30 mV

138 sistently predicted an increase in the rapid delayed rectifier K(+) current and a drastic decrease in

139 H NPY neurons have a large, leptin-sensitive delayed rectifier K(+) current and that leptin sensitivi

140 in HERG (LQT2), the gene encoding the rapid delayed rectifier K(+) current I(Kr), account for a sign

141 tant HERG protein is a mechanism for reduced delayed rectifier K(+) current in LQT2, and high-affinit

142 that form the pore of the rapidly activating delayed rectifier K(+) current in the heart.

143 nnels are responsible for the high threshold delayed rectifier K(+) current typical of Kv2.1.

144 ) current and a drastic decrease in the slow delayed rectifier K(+) current, and this prediction was

145 to calibrate INaL and the rapidly activating delayed rectifier K(+) current, IKr, in the Faber-Rudy c

146 channel conducting the slow component of the delayed rectifier K(+) current, IKs.

147 a-go-go-related gene (HERG), which encodes a delayed rectifier K(+) current.

148 ammonium (TEA) is frequently used to inhibit delayed rectifier K(+) currents (I(DR)) during electroph

149 +) current (I(to)), but not the fast or slow delayed rectifier K(+) currents (I(Kr)/I(Ks)).

150 cts of left ventricular hypertrophy (LVH) on delayed rectifier K(+) currents and their contribution t

151 Delayed rectifier K(+) currents are critical to action p

152 dentifying ICC and in studies of the role of delayed rectifier K(+) currents in ICC functions.

153 n can be detected as a marked enhancement of delayed rectifier K(+) currents in voltage clamp measure

154 lowly (I(Ks)) and rapidly (I(Kr)) activating delayed rectifier K(+) currents were recorded by the who

155 Two delayed rectifier K(+) currents with distinct electrophy

156 ded L- (I(Ca.L)) and T- (I(Ca.T)) type Ca2+, delayed rectifier K+ (I(K)), hyperpolarization-activated

157 oltage-gated K+ channel Kv2.1 is an abundant delayed rectifier K+ (IK) channel expressed at high leve

158 e editing of mRNAs that encode the classical delayed rectifier K+ channel (SqK(v)1.1A) in the squid g

159 (human ether-a-go-go-related gene) encodes a delayed rectifier K+ channel vital to normal repolarizat

160 2+ channel and is not accessible to the slow delayed rectifier K+ channel.

161 assium channels, which typically behave like delayed rectifier K+ channels in other species.

162 In contrast, we found that slow delayed rectifier K+ channels were not changed significa

163 on of Ca2+- and voltage-gated K+ channels or delayed rectifier K+ channels.

164 11.1 alpha-subunit of the rapidly activating delayed rectifier K+ current (IKr) in the heart.

165 e (HERG) give rise to the rapidly activating delayed rectifier K+ current (IKr), the perturbation of

166 units to form channels that conduct the slow delayed rectifier K+ current (IKs) important for repolar

167 sitive (IC50 = 9 mM), iberiotoxin-resistant, delayed rectifier K+ current and a Na+ current inhibited

168 VIP increased delayed rectifier K+ current and L-type calcium current

169 90 rescue was affected by rapidly activating delayed rectifier K+ current blocker consistent with the

170 tent with the increase of rapidly activating delayed rectifier K+ current by lumacaftor is the underl

171 nK assembles with KvLQT1 to produce the slow delayed rectifier K+ current IKs and may assemble with H

172 ntral neurons, is a major contributor to the delayed rectifier K+ current in hippocampal neurons and

173 h KCNE1 to form channels that conduct a slow delayed rectifier K+ current, IKs.

174 -function of the atrial specific ultra-rapid delayed rectifier K+ current, IKur.

175 The role of IKs, the slow delayed rectifier K+ current, in cardiac ventricular rep

176 KCNQ1 channels underlie the slow delayed rectifier K+ current, mediate repolarization of

177 Delayed rectifier K+ currents are involved in the contro

178 We conclude that CaMKII regulates delayed rectifier K+ currents in murine colonic myocytes

179 oltage clamp of isolated myocytes identified delayed rectifier K+ currents that activated rapidly (ti

180 ulted in the activation of a time-dependent, delayed rectifier K+current (IK) in the endothelial cell

181 ion was selectively sensitive to blockers of delayed-rectifier K channels (K(DR)).

182 lpha and PTPepsilon modulate the activity of delayed-rectifier K(+) channels (I(K)).

183 artment included fast-inactivating Na(+) and delayed-rectifier K(+) conductances, while an apical-den

184 otentially arrhythmogenic reductions in slow delayed-rectifier K(+) current (IKs).

185 n rat brain slices showed that GTx inhibited delayed-rectifier K(+) current but not transient A-type

186 Whereas the activation of the delayed-rectifier K(+) current causes bandpass behavior

187 contains an L-type Ca(2+) current, a "rapid" delayed-rectifier K(+) current, a small slowly-activated

188 2+) current, assessment of the role of rapid delayed-rectifier K(+) current, and Ca(2+)-activated K(+

189 mitant inhibition of the rapid or ultrarapid delayed-rectifier K(+) currents (IKr and IKur, respectiv

190 rval prolongation or inhibition of the rapid delayed-rectifier K(+)-current (IKr) encoded by the huma

191 and the reasons for this, the density of the delayed-rectifier K+ current and its two components, i(K

192 Delayed-rectifier K+ currents (I(DR)) in pancreatic beta

193 endent trafficking regulation of the cardiac delayed rectifier KCNQ1/KCNE1 channels.

194 By contrast, delayed rectifier Kv channels (e.g., Kv1.1) and Nav chan

195 dependent Kv2.1 K(+) channels, which mediate delayed rectifier Kv currents (I(K)), are expressed in l

196 voltage-dependent activation of Kv2.1-based delayed-rectifier Kv currents (I(DR)).

197 ne at subsurgical concentrations potentiated delayed rectifier Kv1 channels at low depolarizing poten

198 ngs demonstrate the exquisite sensitivity of delayed rectifier Kv1 channels to modulation by volatile

199 ric channels, but selectively associate with delayed rectifier Kv2 subunits to form heteromeric chann

200 etry of heteromeric channels composed of the delayed rectifier Kv2.1 subunit and the modulatory Kv9.3

201 Delayed-rectifier Kv2.1 potassium channels regulate soma

202 The drug inhibited the delayed rectifier (Kv2) potassium channels from Drosophi

203 alteration in the function or expression of delayed, rectifier (Kv2.1) potassium channels on heterot

204 A similar effect of PIP(2) on the delayed rectifiers Kv7.1 and Kv11.1, two voltage-gated K

205 to the two hMSC models expressing functional delayed rectifier-like human ether a-go-go K+ channel 1

206 s suggest that the modulated currents may be delayed rectifier-like IK.

207 ones results, in part, from an inhibition of delayed rectifier-like IK.

208 dium current (TTX-R I(Na)) and to suppress a delayed rectifier-like potassium current (I(K)).

209 I(h) was caused by its interaction with the delayed-rectifier M-type K(+) current.

210 nels and we categorized them as belonging to delayed-rectifier, M-, D-, or A-type K(+) channels previ

211 fundus ICC, DTX-K blocked a component of the delayed rectifier outward current.

212 inactivating potassium current known as the delayed rectifier plays a major role in membrane repolar

213 ents are modulated by A-like K+ channels and delayed rectifiers (possibly K(V)1.2) but not by Ca(2+)-

214 characterize the properties of variant slow delayed rectifier potassium (I(Ks)) channels identified

215 is the pore-forming subunit of cardiac slow-delayed rectifier potassium (IKs) channels.

216 The delayed rectifier potassium (K(+)) channel KCNB1 (Kv2.1)

217 r taurine in the regulation of voltage-gated delayed rectifier potassium (K(V)) channels in retinal n

218 The regulation of cardiac delayed rectifier potassium (Kv) currents by cAMP-depend

219 d gene (hERG) encodes the rapidly activating delayed rectifier potassium channel (I(Kr)) which plays

220 re-forming subunit of the rapidly activating delayed rectifier potassium channel (I(Kr)).

221 re-forming subunit of the rapidly activating delayed rectifier potassium channel (IKr), which is impo

222 re-forming subunit of the rapidly activating delayed rectifier potassium channel (IKr).

223 the alpha subunit of the rapidly activating delayed rectifier potassium channel (IKr).

224 The cardiac slow delayed rectifier potassium channel (IKs), comprised of

225 ferentiation and the accompanying changes in delayed rectifier potassium channel activity.

226 el, Isk-related family, member 1 (KCNE1) the delayed rectifier potassium channel I(Ks).

227 tions in the gene encoding the voltage-gated delayed rectifier potassium channel Kv1.1 as underlying

228 The Kv2.1 gene encodes a highly conserved delayed rectifier potassium channel that is widely expre

229 HERG encodes the cardiac rapid delayed rectifier potassium channel that mediates repola

230 re-forming subunit of the rapidly activating delayed rectifier potassium channel.

231 e (HERG) that encodes the rapidly activating delayed rectifier potassium channel.

232 Gene transfer of delayed rectifier potassium channels represents a novel

233 assium 2.1 (Kv2.1) channels are the dominant delayed rectifier potassium channels responsible for act

234 ongation of the action potential by block of delayed rectifier potassium channels would be expected t

235 currents (primarily through rapid and slowed delayed rectifier potassium channels) and that block of

236 We found a delayed rectifier potassium conductance that appeared as

237 ed a proportionally larger activation of the delayed rectifier potassium conductance.

238 cement of L-type Ca(2+) current (I(CaL)) and delayed rectifier potassium current (I(K)) in guinea pig

239 m current (I(Ca)) and rapid component of the delayed rectifier potassium current (I(Kr)) by verapamil

240 re-forming subunit of the rapidly activating delayed rectifier potassium current (I(Kr)) important fo

241 channel that conducts the rapidly activating delayed rectifier potassium current (I(Kr)) in the heart

242 yellowfin tunas, through the blocking of the delayed rectifier potassium current (I(Kr)).

243 ibrillation produces an increase of the slow delayed rectifier potassium current (I(Ks)).

244 A developmental increase in delayed rectifier potassium current (I(Kv)) in embryonic

245 ptor subtype and involving inhibition of the delayed rectifier potassium current (I(Kv)).

246 The rapid components of the delayed rectifier potassium current (IKr) and the inward

247 Drugs are screened for delayed rectifier potassium current (IKr) blockade to pr

248 ascribed to inhibition of the cardiac rapid delayed rectifier potassium current (IKr).

249 Effects on the slow delayed rectifier potassium current (IKs) are less recog

250 ng the beta subunit of the slowly activating delayed rectifier potassium current (IKs) channel protei

251 The slow delayed rectifier potassium current (IKs) is a key repol

252 -of-function' mutation, which increases slow-delayed rectifier potassium current (IKs).

253 wo currents with opposing effects: the rapid delayed rectifier potassium current and the L-type calci

254 of LV in the presence of rapidly activating delayed rectifier potassium current blockade.

255 tuated in the presence of rapidly activating delayed rectifier potassium current blockers (E-4031 and

256 Delayed rectifier potassium current diversity and regula

257 ich more closely resemble rapidly activating delayed rectifier potassium current in the human heart,

258 The cardiac delayed rectifier potassium current mediates repolarizat

259 e of the rapidly activating component of the delayed rectifier potassium current) or block multiple i

260 A modulation of I(KS) (slow component of the delayed rectifier potassium current) remained intact.

261 nt, an A-type transient potassium current, a delayed rectifier potassium current, and a muscarinic po

262 zalutamide acutely and chronically inhibited delayed rectifier potassium current, and chronically enh

263 IKs, the slow component of the delayed rectifier potassium current, figures prominently

264 s (transient potassium current, I(K(A)), and delayed rectifier potassium current, I(K(V))) were recor

265 the rapid delayed rectifier potassium current, I(Kr), which flows

266 The 2 components of the delayed rectifier potassium current, IKr (rapid) and IKs

267 The rapidly activating delayed rectifier potassium current, IKr, was studied in

268 the more slowly activating component of the delayed rectifier potassium current, IKs, and using whol

269 In cardiomyocytes, the slowly activating delayed rectifier potassium current, or IKs, is believed

270 iled model of the cardiac rapidly activating delayed rectifier potassium current.

271 by indirect, rate-dependent changes in slow delayed rectifier potassium current.

272 The amplitudes of delayed rectifier potassium currents (I(Kd)) in CA1 neur

273 l cord astrocytes and have demonstrated that delayed rectifier potassium currents (I(Kd)), in particu

274 annels, such as Kv2.1 and SK, which underlie delayed rectifier potassium currents and afterhyperpolar

275 ardiomyocyte model, enDUB treatment restored delayed rectifier potassium currents and normalized acti

276 ng in mammalian neurons requires ultra-rapid delayed rectifier potassium currents generated by homome

277 ides a mechanism for influence over multiple delayed rectifier potassium currents in mammalian CNS vi

278 eased the TRPV1 currents, depressed the slow delayed rectifier potassium currents, and increased the

279 type 1b) expression in rat neurons depresses delayed rectifier potassium currents, limits the magnitu

280 intrinsic conductances, the sodium (gNa) and delayed-rectifier potassium (gK(DR)) channels were found

281 ions in the function and localization of the delayed-rectifier potassium channel, Kv2.1.

282 This also depends on slow delayed-rectifier potassium channels, and preferred thet

283 d neurotransmitter/neuromodulator receptors, delayed-rectifier potassium channels, calcium-dependent

284 cocaine in the heart is a suppression of the delayed-rectifier potassium current (I(K)) that is impor

285 interpretation that, at the cellular level, delayed-rectifier potassium current is a main contributo

286 ier potassium current, the slowly activating delayed-rectifier potassium current, the inward rectifie

287 n currents, including the rapidly activating delayed-rectifier potassium current, the slowly activati

288 KEY POINTS: Kv2 channels underlie delayed-rectifier potassium currents in various neurons,

289 Kv2 channels underlie delayed-rectifier potassium currents in various neurons,

290 Kv2 family "delayed-rectifier" potassium channels are widely express

291 with reduction in the rapid component of the delayed rectifier repolarizing current (I(Kr)).

292 suggest that the four point mutations impair delayed-rectifier type potassium currents by different m

293 A-type Kv4 current to a slowly inactivating delayed rectifier-type potassium current.

294 Delayed-rectifier-type K(+) channels had a single-channe

295 -sensitive currents indicates that they were delayed rectifier types of I(K).

296 function of Kv2.1, the major somatodendritic delayed rectifier voltage-dependent K+ channel in centra

297 A delayed rectifier voltage-gated K(+) channel (Kv) repres

298 The Shaw-like potassium channel Kv3.1, a delayed rectifier with a high threshold of activation, i

299 The current had characteristics of a delayed rectifier with activation positive to -50 mV and

300 ta1.3 subunit converts K(v)1.5 channels from delayed rectifiers with a modest degree of slow inactiva