ライフサイエンスコーパス: potassium current

1 arybdotoxin-sensitive (BK) calcium-dependent potassium current.

2 fied potassium current and transient outward potassium current.

3 equired for generating the transient outward potassium current.

4 which leads to an increase in voltage-gated potassium current.

5 that is mediated by a slow calcium-activated potassium current.

6 hat are mediated by a slow calcium-activated potassium current.

7 ch dictated by a different calcium-dependent potassium current.

8 current and a decrease of transient outward potassium current.

9 cardiac rapidly activating delayed rectifier potassium current.

10 which was attributable to a barium-sensitive potassium current.

11 rols the outward/repolarizing slow rectifier potassium current.

12 vation of bulk calcium inhibits a persistent potassium current.

13 s of voltage-dependent and calcium-dependent potassium current.

14 s that underlie dendrotoxin-sensitive D-type potassium current.

15 xpressions and attenuated the peak of inward potassium current.

16 ontributions to the depolarization-activated potassium current.

17 voltage-dependent contribution to ACh-evoked potassium current.

18 -dependent changes in slow delayed rectifier potassium current.

19 ntrast, NRG1 had minor effects on whole-cell potassium currents.

20 nd the acquisition of mature inner hair cell potassium currents.

21 increased inactivation of voltage-activated potassium currents.

22 r6.2 (I(KATP)) and reducing inward rectifier potassium currents.

23 pe, delayed rectifier, and calcium-dependent potassium currents.

24 cing calcium currents and increasing outward potassium currents.

25 nel gating kinetics of the calcium dependent potassium currents.

26 on as wild-type channels but fail to conduct potassium currents.

27 the fast-inactivating and calcium-activated potassium currents.

28 nce, depolarisation block, and low-threshold potassium currents.

29 slowly rising and falling calcium-dependent potassium currents.

30 DHPG also decreased potassium currents.

31 sion, increased degradation and smaller Kir3 potassium currents.

32 failed to alter holding or voltage-dependent potassium currents.

33 her mechanisms may also lead to reduction of potassium currents.

34 d by calcium-activated, cyclic AMP-sensitive potassium currents.

35 e) cause compensatory decreases in postspike potassium currents.

36 sociated with two distinct calcium-activated potassium currents.

37 bility by reducing BK-type calcium-activated potassium currents.

38 east in part, by decreased Kv7.2/3 (KCNQ2/3) potassium currents.

39 n of a G protein-coupled inwardly rectifying potassium current, (2) inhibition of a voltage-gated Ca(

40 ory processing and that changes in levels of potassium currents across the nuclei, by mechanisms such

41 rane potential hyperpolarized due in part to potassium current activation.

42 d docking simulations we show that the novel potassium current activator, NS5806, binds at a hydropho

43 M-current is a slowly activating potassium current, active at subthreshold potentials.

44 The transient outward potassium current agonist NS5806 (5 muM) and the Ca(2+)-

45 rkably, daily antiphase cycles of sodium and potassium currents also drive mouse clock neuron rhythms

46 ting from reduction of the transient outward potassium current, alters properties of EC coupling.

47 associated with decreased transient outward potassium current and Kv4.2 and KChIP2 protein expressio

48 the Drosophila brain reveal that whole-cell potassium current and properties of single dSlo channels

49 ons express the fast delayed rectifier (FDR) potassium current and raise questions about the function

50 ation via normalization of transient outward potassium current and sarcoplasmic reticulum Ca(2+) cont

51 ion of a large conductance calcium-dependent potassium current and the opening of a transient outward

52 ns across models identified inward rectifier potassium current and the sodium-potassium pump as the t

53 ith blockade of ultrarapid delayed rectified potassium current and transient outward potassium curren

54 v4.2 is a major constituent of A-type (I(A)) potassium currents and a key regulator of neuronal membr

55 2.1 and SK, which underlie delayed rectifier potassium currents and afterhyperpolarization respective

56 are responsible for distinct types of native potassium currents and are associated with several human

57 alretinin cells (85%) exhibited large A-type potassium currents and delayed firing action potential d

58 cells that include inhibition of KIR and KV potassium currents and elevations of intracellular calci

59 used in cancer can prolong QT by inhibiting potassium currents and increasing late sodium current (I

60 toplasmic calcium activated Ca(2+) dependent potassium currents and led to neuronal apoptosis in KO h

61 heir stimulation inhibits M-type [Kv7, K(M)] potassium currents and N-type (Ca(V)2.2) calcium current

62 the functional repertoire of Kv3.1 and Kv3.2 potassium currents and suggest roles for these alpha sub

63 clofenac, dramatically enhanced KCNQ (K(v)7) potassium currents and suppressed L-type voltage-sensiti

64 In na mutants, expression of potassium currents and the key neuropeptide PDF are elev

65 o fourfold interanimal variability for three potassium currents and their mRNA expression.

66 rent, inhibition of a slow calcium-activated potassium current, and activation of a calcium-dependent

67 current was outweighed by calcium-activated potassium current, and in current clamp, nimodipine usua

68 lcium entry and subsequent calcium-activated potassium current, and the hyperpolarizing shift in post

69 delayed firing discharge, large rapid A-type potassium currents, and central, radial or vertical cell

70 and small (SK) conductance calcium-activated potassium currents, and hyperpolarization-activated (I(H

71 rrents, depressed the slow delayed rectifier potassium currents, and increased the resting membrane p

72 elayed repolarization from downregulation of potassium currents, and multiple reentry circuits during

73 POSH decreased potassium currents, and the inhibitory effect of POSH on

74 es in the leak, sodium and calcium-activated potassium currents are central to these two developmenta

75 ased in pathological situations where A-type potassium currents are decreased.

76 A-type potassium currents are important determinants of neurona

77 rom differential expression of voltage-gated potassium currents, as tufted cells exhibited faster act

78 dominant-negative reduction of the resulting potassium current at subthreshold membrane potentials.

79 rrent (I(M)), and may also underlie the slow potassium current at the node of Ranvier, I(Ks).

80 did not affect hERG/IKr or any other cardiac potassium current at therapeutic concentrations.

81 urve (2 voltage sensor mutations) decreasing potassium currents at the subthreshold level at which th

82 In addition to modulating sodium and potassium currents, beta subunits play nonconducting rol

83 ence of rapidly activating delayed rectifier potassium current blockade.

84 ence of rapidly activating delayed rectifier potassium current blockers (E-4031 and cisapride), incre

85 We observed large voltage-dependent potassium currents, but only a small chromanol sensitive

86 ly because of lack of inhibition of the I(A) potassium current by ERK.

87 Background potassium currents carried by the KCNK family of two-por

88 gets, including the I(Ks) (slowly activating potassium current) channel.

89 y (HEK) 293 cells produced a noninactivating potassium current characteristic of M current.

90 GS and GLAST expressions and enhanced inward potassium currents compared with those in the COH rats w

91 Taken together these data indicate that potassium currents constitute a basic determinant for C.

92 positive membrane potential, the ACh-evoked potassium current decayed exponentially over approximate

93 We observed reduced sodium and potassium current densities in ventricular myocytes, as

94 Pergolide inhibited PASMC potassium current density, resulting in membrane depolar

95 The balance between two particular potassium currents dictates how heart cells respond to p

96 Individual neurons with different levels of potassium currents differ in their ability to follow spe

97 ings are consistent with the hypothesis that potassium current downregulation leads to abnormal repol

98 lock phase involve persistent suppression of potassium current, downstream of Per1 gene induction, in

99 esults from frequency-dependent reduction of potassium current during spike repolarization.

100 Inactivation of potassium currents during maintained firing results in a

101 e M-current, a low-threshold noninactivating potassium current, during seizures.

102 the G protein-activated inwardly-rectifying potassium current evoked by receptor-saturating concentr

103 ting the duration of the AP, the BK-mediated potassium current exerts control over the frequency of A

104 ll-cell coupling lead to regional changes in potassium current expression, which in this case facilit

105 Reduced inward potassium current following nerve ligation would increas

106 Noninactivating potassium current formed by KCNQ2 (Kv7.2) and KCNQ3 (Kv7

107 They are responsible for background leak potassium currents found in many cell types.

108 patch-clamp techniques, recordings of either potassium current from rat posterior taste receptor cell

109 contact sites and has been shown to regulate potassium current gating kinetics as well as channel tra

110 non-inactivating low-threshold voltage-gated potassium current generated by the M-channel.

111 urons requires ultra-rapid delayed rectifier potassium currents generated by homomeric or heteromeric

112 Potassium currents generated by voltage-gated potassium

113 he magnitude of fast delayed rectifier (FDR) potassium currents has a diurnal rhythm that peaks durin

114 f-function mutations in the gene for outward potassium currents have been shown to underlie the conge

115 , we evaluated whether the transient outward potassium current I(A) is expressed in PVN-RVLM neurones

116 often caused by direct block of the cardiac potassium current I(Kr)/hERG, which is crucial for termi

117 ed most often by direct block of the cardiac potassium current I(Kr)/hERG.

118 Apamin sensitive potassium current (I KAS), carried by the type 2 small c

119 A-type potassium current (I(A)) both activates and inactivates

120 med to address whether the transient outward potassium current (I(A)) in identified rostral ventrolat

121 hat DA could immediately alter the transient potassium current (I(A)) of identified neurons in the st

122 dine and 0.5 mM Ba2+, consistent with A-type potassium current (I(A)).

123 n the time course of acetylcholine-activated potassium current (I(K)(ACh)) activation and deactivatio

124 a(2+) current (I(CaL)) and delayed rectifier potassium current (I(K)) in guinea pig SAN pacemaker cel

125 (I(Na)) and 4AP-sensitive and TEA-resistant potassium current (I(K)).

126 a)) and to suppress a delayed rectifier-like potassium current (I(K)).

127 ynaptic integration: a low-voltage-activated potassium current (I(K-LVA)) and a hyperpolarization-act

128 n important role for the inwardly rectifying potassium current (I(K1)) in controlling the dynamics of

129 rrent mechanisms are the inwardly rectifying potassium current (I(K1)), which is important for mainte

130 ductance differences in the inward rectifier potassium current (I(K1)).

131 hannels mediate the cardiac inward rectifier potassium current (I(K1)).

132 ally depended on the expression of an A-type potassium current (I(KA)), which when active attenuated

133 recorded block by lopinavir of repolarising potassium current (I(Kr)) channels in neonatal mouse car

134 hrough the blocking of the delayed rectifier potassium current (I(Kr)).

135 es an increase of the slow delayed rectifier potassium current (I(Ks)).

136 cAMP-dependent increase in the slow outward potassium current (I(Ks)).

137 Kv1.5 mediates the ultrarapid potassium current (I(Kur)) that controls atrial action p

138 nnels contributing to the ultrarapid outward potassium current (I(Kur)).

139 pression would predict different patterns of potassium current (I(Kv)) regulation.

140 nvolving inhibition of the delayed rectifier potassium current (I(Kv)).

141 heterogeneous loss of the transient outward potassium current (I(to))-mediated epicardial action pot

142 sed the inward and delayed outward rectifier potassium currents (I IRK and I DRK), calcium (Ca2+) rel

143 neurons, the amplitude of rapid inactivating potassium currents (I(A)) was significantly increased at

144 ge-dependent activation of voltage-sensitive potassium currents (I(K)).

145 treatment with blockers of calcium-activated potassium currents (I(KCa)) reproduced this shift and bl

146 The amplitudes of delayed rectifier potassium currents (I(Kd)) in CA1 neurons were progressi

147 t a novel coupled system of sodium-activated potassium currents (I(KNa)) and persistent sodium curren

148 that contribute to cardiac transient outward potassium currents (I(to)).

149 sing cultured DRG neurons, that of the total potassium current, I(K), the K(Na) current is predominan

150 the rapid delayed rectifier potassium current, I(Kr), which flows through the human

151 pid compensatory interaction among a pair of potassium currents, I(A) and I(KCa), that stabilizes bot

152 ltage-clamp experiments, 2-AG reduced A-type potassium current (IA) through a cannabinoid receptor-in

153 GxTX-1E also reduced A-type potassium current (IA), but much more weakly.

154 by the opposing actions of the fast outward potassium current, IA , mediated by alpha subunits of th

155 lux (IC(50), 1.4 nM) and inwardly rectifying potassium currents (IC(50), 1 nM) in CHO cells stably ex

156 system underlying the ultra-rapid rectifying potassium current (Ik(ur)), a major repolarizing current

157 solated CB preparation and decreased outward potassium current (Ik) in CB glomus cells to levels simi

158 pendent, time-independent rectifying outward potassium current (IK).

159 In each neuron, voltage-dependent potassium currents (IK) were evaluated and, in represent

160 25 microM) also suppressed voltage-activated potassium currents (IK+) and calcium currents (ICa2+).

161 lum Ca2+ concentrations, inwardly rectifying potassium current (IK1) density, and gap junction conduc

162 mulations predict that the inward rectifying potassium current (IK1) is an essential determinant of r

163 ssium current (IKr) and the inward rectifier potassium current (IK1) were also downregulated (P<0.05)

164 Delayed excitation, caused by A-type potassium current (IKA), was observed in most of NTS neu

165 armacological tools, acetylcholine-regulated potassium current (IKACh) with patch clamp recording, me

166 paper unveils the critical role of the brake potassium current IKD in damage-triggered cold allodynia

167 A low voltage-activated potassium current, IKL, is found in auditory neuron type

168 utational modeling, that a low-voltage-gated potassium current, IKLT, underlies the resonance.

169 he rapid components of the delayed rectifier potassium current (IKr) and the inward rectifier potassi

170 Drugs are screened for delayed rectifier potassium current (IKr) blockade to predict long QT synd

171 ition of the cardiac rapid delayed rectifier potassium current (IKr).

172 and KCNE1 protein coassembly forms the slow potassium current IKS that repolarizes the cardiac actio

173 KCNE1, Kv7.1 conducts the slowly activating potassium current IKs, which is one of the major current

174 Effects on the slow delayed rectifier potassium current (IKs) are less recognized.

175 ate the slowly activating, voltage-dependent potassium current (IKs) in the heart that controls the r

176 The slow delayed rectifier potassium current (IKs) is a key repolarizing current du

177 tion, which increases slow-delayed rectifier potassium current (IKs).

178 l, IKr, and the adrenergic-sensitive cardiac potassium current, IKs, are two primary contributors to

179 potassium channel and its associated cardiac potassium current, IKur.

180 foundly altered protein function, inhibiting potassium current in a dose-dependent manner.

181 that SNX-482 dramatically reduced the A-type potassium current in acutely dissociated dopamine neuron

182 Dysfunction of the fast-inactivating Kv3.4 potassium current in dorsal root ganglion (DRG) neurons

183 ily underlie a major component of the A-type potassium current in mammalian central neurons.

184 Moreover, POSH still decreased the potassium current in oocytes injected with a ROMK1 mutan

185 nsitization of the mu-opioid receptor-evoked potassium current in rat locus ceruleus neurons.

186 (rs1805128), known to modulate an important potassium current in the heart, predicted diLQTS with an

187 The largest outward potassium current in the soma of neocortical pyramidal n

188 tamine produced a dose-dependent increase in potassium currents in a subset of bipolar cells.

189 The present study compared the changes of potassium currents in acutely dissociated hippocampal ne

190 Low-threshold potassium currents in deprived NM neurons were not signi

191 n resulted in lack of time-dependent outward potassium currents in guard cells, higher rates of water

192 n previously shown to modulate voltage-gated potassium currents in heterologous expression systems.

193 results indicated that the voltage dependent potassium currents in hippocampal neurons were different

194 ion potential waveforms, and reduced outward potassium currents in isolated cardiac myocytes.

195 Potassium currents in olfactory bulb mitral cells from K

196 ression of CD63 had no significant effect on potassium currents in oocytes injected with ROMK1; howev

197 strated MYOCD-induced, iberiotoxin-sensitive potassium currents in porcine coronary SMCs.

198 d by reductions in BK-type calcium-activated potassium currents in spontaneously firing neurons, is e

199 e data support two highly novel conclusions: potassium currents in taste receptor cells are significa

200 we investigated Kv3.1b immunoreactivity and potassium currents in the auditory brainstem sound local

201 Leak potassium currents in the nervous system are often carri

202 By enhancing potassium currents in the ON bipolar cells, histamine is

203 H at 5 microM increased the amplitude of the potassium currents in the ON bipolar cells.

204 el mechanism for regulation of voltage-gated potassium currents in the setting of cardiac pathology a

205 NTS: Kv2 channels underlie delayed-rectifier potassium currents in various neurons, although their ph

206 Kv2 channels underlie delayed-rectifier potassium currents in various neurons, although their ph

207 al evidence that the mutant protein disrupts potassium current inactivation, strongly supports KCND2

208 In voltage clamp mode, the sodium and potassium currents increased significantly at higher [Na

209 regulated Kcna2, reduced total voltage-gated potassium current, increased excitability in DRG neurons

210 neurons in the locus ceruleus to measure the potassium current induced by morphine.

211 ctions) does not affect the extent of M-type potassium current inhibition produced by either receptor

212 at, at the cellular level, delayed-rectifier potassium current is a main contributor of KECG correlat

213 evidence that opposite regulation of A-type potassium current is an important factor in this bidirec

214 er, a mutation that impairs Shaker-dependent potassium current, is an allele of sleepless.

215 I(Ks), the slow heart potassium current, is carried by the I(Ks) potassium cha

216 bunit in somatodendritic subthreshold A-type potassium current (ISA) channels.

217 gnificant reduction of the transient outward potassium current (Ito) in EPI but not in endocardial (E

218 The fast transient outward potassium current (Ito,f) plays a critical role in the e

219 revealed downregulation of transient outward potassium current (Ito; P<0.05).

220 tagonized by activators of the ATP-sensitive potassium current (K(ATP)).

221 rpolarization-activated, inwardly rectifying potassium current (K(IR)).

222 the supernormal phase results from a reduced potassium current Kdr as a result of accumulation of per

223 on onsets were regeneratively amplified by a potassium current (KIR) whose activation promoted furthe

224 genes (hERG), which encode two repolarizing potassium currents known as I(Ks) and I(Kr).

225 Thus, a potassium current, likely mediated through BK channels,

226 n in rat neurons depresses delayed rectifier potassium currents, limits the magnitude of the K+ curre

227 ctive" mutations affecting calcium-dependent potassium currents localized to the C-domain of CaM.

228 BA(A) current and an intrinsic membrane slow potassium current (M-current).

229 hrough G-protein coupled inwardly rectifying potassium currents mediated by delta and mu opioid recep

230 e rat hippocampal slices we show that D-type potassium current modulates the size of the ADP and the

231 y consistent reductions in voltage-activated potassium currents near the action potential threshold a

232 lective, as NS5A1a does not depress neuronal potassium currents nor inhibit Src phosphorylation of Kv

233 led that the isoflurane-activated background potassium current observed in cortical pyramidal neurons

234 ion was mediated by activation of an outward potassium current or blockade of a tonically active inwa

235 tes, the slowly activating delayed rectifier potassium current, or IKs, is believed to be a heteromul

236 e two calcium channels and acting on the two potassium currents, or with differences in channel gatin

237 ation of the MOR and reduced activation of a potassium current over the same time course.

238 CHO-K1 cells line produces highly selective potassium current, overexpression of R162W mutant Kir7.1

239 In the evening, basal potassium currents peak to silence clock neurons.

240 tassium current, the acetylcholine activated potassium current, peak sodium current, and L-type calci

241 le (CG) cells and many other neurons, A-type potassium currents play an important role in regulating

242 the major cause of ischemic cell death, and potassium currents play important roles in regulating th

243 Importantly, A-type potassium currents recorded in mesoaccumbal neurons disp

244 t reduction, but the contribution to overall potassium current reduction was almost always much small

245 KS) (slow component of the delayed rectifier potassium current) remained intact.

246 age dependence of acetylcholine (ACh)-evoked potassium currents reveal a more complex relationship be

247 pression of KCNQ1-S140G with KCNE1 generated potassium currents (S140G-IKs) that exhibited greater se

248 -calcium exchanger activity, reduced outward potassium currents, sarcoplasmic reticulum Ca2+ defects,

249 ese is an apamin-sensitive calcium-dependent potassium current (SK).

250 nvolving small conductance calcium-dependent potassium currents (SK).

251 n of the small conductance calcium-activated potassium current, SK.

252 idal neurones we studied the modulation of a potassium current (slow AHP current, I(sAHP)) known to b

253 nce of calcium current and calcium-activated potassium current such that their net influence shifted

254 ent is a slowly activating, non-inactivating potassium current that has been shown to be present in n

255 , there was a component of calcium-dependent potassium current that showed frequency-dependent reduct

256 Since Hodgkin and Huxley discovered the potassium current that underlies the falling phase of ac

257 These channels produce background leak type potassium currents that act to regulate resting membrane

258 licited increases of the inwardly rectifying potassium currents that could be blocked by the GABA(B)

259 tal cholinergic interneurons are sculpted by potassium currents that give rise to prominent afterhype

260 fier potassium current, the inward rectifier potassium current, the acetylcholine activated potassium

261 ent, the slowly activating delayed-rectifier potassium current, the inward rectifier potassium curren

262 ing the rapidly activating delayed-rectifier potassium current, the slowly activating delayed-rectifi

263 Expression of one important potassium current, the transient outward current (I(to))

264 ny medications inadvertently block the KCNH2 potassium current, these novel findings seem to have cli

265 The ability of crotamine to inhibit the potassium current through K(V) channels unravels it as t

266 Potassium currents through SK channels demonstrate inwar

267 channel 3, where SP enhances M-channel-like potassium currents through the NK1 receptor in a G prote

268 fort, a molecular-level understanding of the potassium current underlying the slow afterhyperpolariza

269 Little is known about the voltage-dependent potassium currents underlying spike repolarization in mi

270 selectively coupled to the calcium-dependent potassium currents underlying the AHPs, thereby creating

271 molecular correlate of the transient outward potassium current up-regulated by Abeta peptide, conside

272 specifically enhances an inwardly rectifying potassium current via NPY-Y1 receptors.

273 naptic efficacy, inhibiting postsynaptic Kv3 potassium currents (via phosphorylation), reducing EPSCs

274 Reduction of potassium current was also seen with multimeric G85R SOD

275 Although this potassium current was described two decades ago, the mec

276 dent reduction of overall spike-repolarizing potassium current was identified as Kv3 current by its s

277 The potassium current was inhibited by 4-AP and by Heteropod

278 ion of G protein-coupled inwardly rectifying potassium current was measured using whole-cell voltage-

279 The effect of cross-linked 300 kDa on potassium current was reduced by removing Na(+) from the

280 tivation kinetics of D(2) receptor-dependent potassium current was studied using outside-out patch re

281 ution of afferent neuronal voltage-dependent potassium currents was a prominent feature of urethral a

282 nd the effects of these analogues on outward potassium current were evaluated by using two electrode

283 Whole-cell recordings of potassium currents were made from bipolar cells in slice

284 The major potassium currents were not different in LDLr(-/-) and A

285 Potassium currents were recorded using 2-microelectrode

286 In 10 mM TEA, potassium currents were reduced in all the bipolar cells

287 In contrast, outward potassium currents were significantly reduced by microin

288 Other potassium currents were spared, except to the extent tha

289 ntrast, depolarization-activated calcium and potassium currents were unaffected, thus supporting the

290 nts ("calcium sparks") and voltage-dependent potassium currents were unaffected.

291 his current matched that of the native Slack potassium current, which was identified using an siRNA a

292 with specific ionic currents, such as A-type potassium currents, which can linearize the frequency-in

293 ity may be limited by the presence of A-type potassium currents, which limit the effectiveness of the

294 nd sustained as well as rapidly inactivating potassium currents, which were sensitive to TEA and 4-AP

295 d of SK (small-conductance calcium-activated potassium) currents, which were essential for a wide lin

296 KCNQ channels might also contribute to this potassium current whose molecular identity is unknown.

297 tween sodium current and inwardly rectifying potassium current with increasing field strength.

298 ive rise to the M-current, a noninactivating potassium current with slow kinetics.

299 mulation, which regulate cardiac calcium and potassium currents with differential kinetics.

300 ffect of POSH on ROMK1 channels, we measured potassium currents with electrophysiological methods in