ライフサイエンスコーパス: voltage dependence

1 Cx26 equivalent region reduced the slow gate voltage dependence.

2 on without significantly altering the pump's voltage dependence.

3 evealed dramatic alterations of kinetics and voltage dependence.

4 ed significant hyperpolarizing shifts in the voltage dependence.

5 selectivity, and only subtle differences in voltage dependence.

6 ge-gated sodium channel Nav and modifies its voltage dependence.

7 been attributed to fast kinetics and strong voltage dependence.

8 of both slow Mg(o)(2+) unblock and inherent voltage dependence.

9 ent of EAG inactivation without altering its voltage dependence.

10 activated with iloprost showed no detectable voltage dependence.

11 hibition but not the PIP(2)-induced shift in voltage dependence.

12 ess changes, displaying the largest shift in voltage dependence.

13 duced more subtle negative shifts in K(V)2.1 voltage dependence.

14 or-like domain, accounting for its deficient voltage dependence.

15 ggests a closed pore consistent with extreme voltage dependence.

16 of lysine 41 with glutamate 42 maintains the voltage dependence.

17 probability of nonlocal manipulation have a voltage dependence.

18 on, however, was weak compared with beta1-AR voltage-dependence.

19 (2)(+) current density without affecting its voltage-dependence.

20 ion, and desensitization kinetics as well as voltage-dependence.

21 ed a half-activation at -79.6 mV and a steep voltage dependence (2.8 mV).

22 that the mutation hyperpolarizes activation voltage dependence (8 mV by manual profiling, 11 mV by r

23 fied reconstituted M-currents, altered their voltage dependence, accelerated activation, and slowed d

24 ed maximum currents and steepnesses in their voltage dependences after addition of the Epac activator

25 Using voltage-dependence analysis of steady-state and transien

26 sociated IKs channel mutations shift channel voltage dependence and accelerate channel closing.

27 Furthermore, Kv1.2 voltage dependence and activation threshold were reduced

28 t on M channel activity, a negative shift in voltage dependence and an increase of the maximal curren

29 The voltage dependence and fast kinetic components in the ac

30 benzimidazoles blocked the negative shift in voltage dependence and increase in amplitude of the calc

31 a(2+)-activated Cl(-) currents with time and voltage dependence and inhibitor sensitivity that resemb

32 receptor currents with low affinity and weak voltage dependence and is effective when applied to rest

33 he VSD operation in Ci-VSP exhibits original voltage dependence and kinetics compared to ion channels

34 v11.3 channels, but altered the steady-state voltage dependence and kinetics of activation in neurona

35 at the prepulse has no visible effect on the voltage dependence and kinetics of Na(+) currents elicit

36 annels on the SMT critically depended on the voltage dependence and kinetics of the calcium sources w

37 nd sustained potassium currents, and altered voltage dependence and kinetics of transient currents.

38 segment and nodal M-currents were similar in voltage dependence and kinetics, carried by K(v)7.2/7.3

39 C) and eM that evidence disparities in their voltage dependence and magnitude as a function of intrac

40 n Kv4 channel complex inactivation kinetics, voltage dependence and recovery.

41 g mice, we measured the amplitude, kinetics, voltage dependence and short-term plasticity of mossy fi

42 mbrane potentials, but also left-shifted its voltage dependence and slowed inactivation.

43 ation of synapses, but it does influence the voltage dependence and strength of Ca(2+) influx at pres

44 The properties of the force generator, its voltage dependence and susceptibility to salicylate, as

45 Currently, the individual voltage dependence and the contribution to pore opening

46 ied BK channels in dopamine neurons by their voltage dependence and their response to a BK channel bl

47 fluorophores, as evidenced by changes in the voltage dependence and time course of DeltaF.

48 The voltage dependence and timing of Ca(2+) entry are though

49 ovement into two steps with widely different voltage dependences and kinetics.

50 nt (QON) of Cav1.3L displayed a much steeper voltage-dependence and a more negative half-maximal acti

51 t, slower apparent dissociation rate, weaker voltage dependence, and complete competition by magnesiu

52 (ICRAC) were identified by ion permeability, voltage dependence, and sensitivity to selective Orai an

53 a glutamate in the same region decreased the voltage dependence, and the neutralization of a negative

54 domain-CNBHD interaction with the kinetics, voltage-dependence, and ATP-dependence of VDP.

55 Mutation-induced changes in channel voltage dependence are most often inferred from macrosco

56 tin, linear capacitance (Clin) also displays voltage dependence as motors move between expanded and c

57 resulted in transport currents with the same voltage dependence as the wild type.

58 roperties lead to pinched hysteretic current-voltage dependence as well a classic dependence of magne

59 Drug efficacy is a major target of beta1-AR voltage-dependence as depolarization attenuated receptor

60 e to promote channel opening with FL(4)-like voltage dependence at depolarizing potentials, but all f

61 The simulations indicate a lower voltage dependence at negative potentials of the kidney

62 P259R inverts the voltage dependence, changes the sodium dependence, and a

63 sensitive ICa (ICa-ins) with a right-shifted voltage dependence compared to that in control fibres.

64 Furthermore, voltage dependence did not derive from association of DP

65 d for proton-activated channels, and current-voltage dependence did not show any differences between

66 conclude that despite subtle differences in voltage dependence, during physiologic activity, blocker

67 GluN1/2B receptors exhibited equal inherent voltage dependence; faster Mg(o)(2+) unblock from GluN1/

68 s in channel gating by shifting (~15 mV) the voltage dependence for steady-state activation and inact

69 ky integrate-and-fire models using a shallow voltage-dependence for the exponential term that matches

70 zine decreased pressure-induced shift in the voltage dependence (IC(50) 54 mumol/L) and eliminated th

71 AT1 anion currents display normal ligand and voltage dependence in cells internally dialyzed with Na(

72 The mechanism of transport coupling and voltage dependence in ClC-5 is unclear.

73 SRCa2+ release also displayed right-shifted voltage dependence in fibres expressing EGFP-alpha1sDHPR

74 n of HCN4 function by depolarizing the basal voltage dependence in the absence of cAMP.

75 ere investigated for their effectiveness and voltage dependence in the inhibition of responses evoked

76 n integrals of gating current, 2) saturating voltage dependence in the Q(charge)-voltage curve, and 3

77 The greater degree of voltage-dependence in Kv4.3 occurs because it is the vol

78 we demonstrate that covarying I(A) and I(H) voltage dependences increases the dynamic range of rebou

79 pair mutant D451E exhibited a right-shifted voltage dependence, indicating an increased apparent aff

80 t sodium-dependent transient currents with a voltage-dependence indicative of an increased apparent a

81 The voltage dependence is enhanced at high extracellular Na(

82 und a membrane potential of zero, negligible voltage dependence is observed because the voltage-indep

83 were slowed down by a factor of 3.5, and the voltage dependence is shifted by 10 mV toward depolarize

84 In HCN, the polarity of voltage dependence is uniquely reversed.

85 rate that this cell-to-cell covariability of voltage dependences is sensitive to cytosolic cAMP and c

86 This voltage-dependence is also transmitted to G protein and

87 This unique voltage dependence makes the dinoflagellate proton chann

88 as an important determinant of the channels' voltage dependence, making the extracellular linkers ess

89 Therefore, we speculate that voltage dependence may arise from interactions of DPA wi

90 The HCN channel exhibits reversed voltage dependence, meaning it closes with depolarizatio

91 calcium-permeable glutamate receptors with a voltage-dependence mediated by blockade by Mg(2+) .

92 n effect by positive-shifting the activation voltage dependence, most likely through a direct effect

93 However, the time and voltage dependence of acetylcholine (ACh)-evoked potassi

94 channel gating with a positive shift in the voltage dependence of activation and altered kinetics of

95 erpolarizing ( approximately 70 mV) shift of voltage dependence of activation and an acceleration of

96 KCNQ1/KCNE1 channels had a positive shift in voltage dependence of activation and an increase in deac

97 SGK1.1 failed to modify the voltage dependence of activation and did not change acti

98 ability of slow inactivation and shifted the voltage dependence of activation and fast inactivation t

99 The antibodies shift the voltage dependence of activation and slow the deactivati

100 +) current (IKs ) by negatively shifting the voltage dependence of activation and slowing deactivatio

101 The effects of Rg3 on the voltage dependence of activation and the deactivation ra

102 urface expression of CaV1.2 protein, and the voltage dependence of activation and the kinetics of ina

103 The voltage dependence of activation and the number of Ca(2+

104 of the relationship between the shift in the voltage dependence of activation and the number of mutat

105 ng altered current density and shifts in the voltage dependence of activation and/or inactivation, as

106 s by 27+/-18% and 18+/-4% and hyperpolarized voltage dependence of activation by -11 mV and -10 mV, r

107 nown to induce a hyperpolarized shift in the voltage dependence of activation in Nav1.7.

108 8 produce a marked shift in the BK channel's voltage dependence of activation in the hyperpolarizing

109 ficacy of an M channel enhancer to shift the voltage dependence of activation may be most important f

110 corpion beta-toxins, Lqh-dprIT(3) shifts the voltage dependence of activation of BgNa(v) channels exp

111 imulate gating and the effects of Rg3 on the voltage dependence of activation of hELK1 channels.

112 causes a rapid hyperpolarizing shift in the voltage dependence of activation of Kv2.1, typical of Ca

113 SNX-482 produced a depolarizing shift in the voltage dependence of activation of Kv4.3 channels and s

114 ncentration of Ca(2+) or Mg(2+) reverted the voltage dependence of activation of the IEM mutant to ne

115 ed an additional 20-mV negative shift in the voltage dependence of activation of toxin-modified chann

116 A mere 5 mV depolarizing shift in the voltage dependence of activation or a hyperpolarizing sh

117 No differences in the voltage dependence of activation or inactivation were de

118 d hNaV1.7 without significantly altering the voltage dependence of activation or inactivation.

119 -mediated changes in activation kinetics and voltage dependence of activation require interaction of

120 Mutations of the beta-strand shift the voltage dependence of activation to more depolarized vol

121 e potentiation is observed as a shift in the voltage dependence of activation to more depolarized vol

122 ets of beta-scorpion toxins, which shift the voltage dependence of activation to more negative membra

123 by inhibiting inactivation and shifting the voltage dependence of activation to more negative potent

124 e maximal current amplitude and shifting the voltage dependence of activation to more positive potent

125 promote the open conformation, shifting the voltage dependence of activation to the negative directi

126 -delimited manner and induces a shift of the voltage dependence of activation toward negative voltage

127 d channel function with a right shift in the voltage dependence of activation, a reduced current dens

128 on mutation, with a hyperpolarizing shift in voltage dependence of activation, a two-fold increase of

129 stitutively active component, hyperpolarized voltage dependence of activation, and extremely slow dea

130 activated tail IKs , negatively shifted the voltage dependence of activation, and slowed deactivatio

131 found HCN4 mutations showed a more negative voltage dependence of activation, consistent with the ob

132 essed in frog oocytes revealed shifts in the voltage dependence of activation, including altered acti

133 onists is related to a leftward shift in the voltage dependence of activation, increasing the probabi

134 so play an important role in fine-tuning the voltage dependence of activation, regulating slow deacti

135 ing, including a hyperpolarized shift in the voltage dependence of activation, slower activation, and

136 when associated with BK-beta1 (left-shifted voltage dependence of activation, V(1/2) = -55 mV, 12 um

137 n immediate hyperpolarizing shift in PD I(A) voltage dependence of activation, whereas tonic DA persi

138 large hyperpolarizing shift (-18 mV) in the voltage dependence of activation.

139 produces a 5.8-mV depolarizing shift in the voltage dependence of activation.

140 (I(NaP)) and a hyperpolarizing shift in the voltage dependence of activation.

141 tage- and calcium-dependent inactivation and voltage dependence of activation.

142 the presence of KCNE1 by right-shifting the voltage dependence of activation.

143 prisingly, a 30 mV depolarizing shift in the voltage dependence of activation.

144 nnel gating by producing a left shift in the voltage dependence of activation.

145 This voltage sensor is crucial for the voltage dependence of agonist binding to the receptor.

146 This strong voltage dependence of alpha2 pumps also helps explain ho

147 CCt induced a depolarizing shift in the voltage dependence of both CaV1.2 current activation and

148 ](i)) induced a hyperpolarizing shift in the voltage dependence of both channel opening and VSD activ

149 A remaining 10-15 mV negative shift in the voltage dependence of both the kinetics and the charge m

150 he S218L mutation causes a negative shift of voltage dependence of Ca(V)2.1 channels of mouse Purkinj

151 The voltage dependence of Ca(V)2.2 inhibition was examined u

152 whole-cell Ca2+ current amplitude, modified voltage dependence of Ca2+ channel activation and attenu

153 However, 92CCt shifted the voltage dependence of CaV1.2 activation and inactivation

154 The voltage dependence of Cd(2+) block of VACCs accounts for

155 mportant role in regulating the kinetics and voltage dependence of channel activation and deactivatio

156 ge negative shift ( approximately 140 mV) in voltage dependence of channel activation.

157 s accompanied by a depolarizing shift in the voltage dependence of channel activation.

158 main, causing a hyperpolarizing shift in the voltage dependence of channel activation.

159 n (CDI) and to cause a positive shift in the voltage dependence of channel activation.

160 rease in peak I(Kv11.1) density, whereas the voltage dependence of channel gating became WT-like.

161 It changes the voltage dependence of channel gating little.

162 e from interactions of DPA with the inherent voltage dependence of channel gating.

163 al analysis reveals that p.V1184A shifts the voltage dependence of channel opening to hyperpolarized

164 we comparatively evaluate the magnitude and voltage dependence of chloride currents (ICl), as well a

165 ometry, we have investigated the calcium and voltage dependence of conformational changes of the gati

166 ablish the relationship between PIP2 and the voltage dependence of cortical KCNQ channels (KCNQ2/3, K

167 The voltage dependence of cotransport and presteady-state ch

168 ontrast, captures the characteristics of the voltage dependence of deltaCsa, leading to a better unde

169 unlike retigabine, SF0034 did not shift the voltage dependence of either KCNQ4 or KCNQ5 homomeric ch

170 In addition, the voltage dependence of ENaC with PHA-1 substitutions is a

171 inal residue that regulates the kinetics and voltage dependence of fast inactivation in sodium channe

172 Lacosamide induced a reversible shift in the voltage dependence of fast inactivation studied with 100

173 Our results suggest that this complementary voltage dependence of GABA(B)/KIR and NMDA conductances

174 In contrast, the midpoints of the voltage dependence of gCa, Q and Ca2+ release were not d

175 urrent density was 62% lower in BCs, and the voltage dependence of gNa inactivation was 13 mV hyperpo

176 Then, we examined the voltage dependence of GV-58 effects on Ca(2+) channels u

177 Here we reverse the voltage dependence of HCN channels by mutating only two

178 bits the canonical depolarizing shift in the voltage dependence of HCN4 in response to the binding of

179 half of the maximal RPR-induced shift in the voltage dependence of hERG1 inactivation, and maximal ef

180 To validate the method, we analyzed the voltage dependence of high- and low-voltage-gated Ca(2+)

181 We evaluated the voltage dependence of human cardiac NKA isozymes express

182 e changes accompanied negative shifts in the voltage dependence of I(Na) inactivation (within 10 min)

183 nt" (If), and a hyperpolarizing shift in the voltage dependence of If.

184 chniques to investigate the [H]o, [Na]o, and voltage dependence of IH in Na/K pumps from ventricular

185 s a significant hyperpolarizing shift in the voltage dependence of inactivation and seems to promote

186 so had a marked hyperpolarizing shift in its voltage dependence of inactivation as well as slowed ina

187 slow component of current decay and shifted voltage dependence of inactivation toward more negative

188 ane potentials due to its unusually negative voltage dependence of inactivation.

189 f an intracellular factor that modulates the voltage dependence of inactivation.

190 e reversal strongly altered the kinetics and voltage dependence of inactivation.

191 st these ideas, we compared the kinetics and voltage dependence of ionic activation and deactivation

192 ted mutation KCNE5-L65F negative shifted the voltage dependence of K(V)2.1-KCNE5 channels, increasing

193 at S4 induces a large depolarizing shift in voltage dependence of K(v)7.2 channels and L268F at the

194 CNE1 coexpression dramatically separates the voltage dependence of KCNQ1/KCNE1 current and fluorescen

195 MIT1 also altered the gating kinetics and/or voltage dependence of KCNQ2, KCNQ2/3, and KCNQ1-KCNE1.

196 more potent than retigabine at shifting the voltage dependence of KCNQ2/3 channels to more negative

197 d a significant hyperpolarizing shift in the voltage dependence of Kv2.1 but had no effect on the fun

198 This reduction is due to a shift in the voltage dependence of Kv7 channel activation to more pos

199 pharmacological manipulation that shifts the voltage dependence of Kv7 to more negative voltages prev

200 roduces immediate depolarizing shifts in the voltage dependence of LP I(A), whereas tonic nanomolar D

201 nt regulator of NMDARs, and particularly the voltage dependence of Mg(2+) block is crucial to the rol

202 Physiological measurements exploiting the voltage dependence of monosynaptic EPSCs similarly indic

203 n the presence of morphine, the steady-state voltage dependence of Na channels was shifted to the lef

204 mplitude, and a hyperpolarizing shift in the voltage dependence of Nav channel steady-state inactivat

205 A(A)Rs that closely matched the kinetics and voltage dependence of NMDARs.

206 ies of IKir and TTS voltage records, and the voltage dependence of peak IKir, while measured at widel

207 The analysis of the source-drain voltage dependence of photocurrent spectra reveals excit

208 However, KCNE3 shifts the voltage dependence of S4 movement to extreme hyperpolari

209 t promoted slow inactivation and shifted the voltage dependence of slow inactivation in the direction

210 tical neurons in awake mice, we measured the voltage dependence of spontaneous voltage fluctuations a

211 Although the voltage dependence of SR calcium release was not statist

212 nactivation, and a depolarizing shift in the voltage dependence of steady-state fast inactivation.

213 ial reactions to cooperatively determine the voltage dependence of steady-state glutamate uptake and

214 lts in a marked hyperpolarizing shift in the voltage dependence of steady-state inactivation of the N

215 inactivation, and a less positively shifted voltage dependence of steady-state inactivation.

216 The voltage dependence of the 4-AP block and the single bind

217 ctivate and potentiate TRPV1 by shifting the voltage dependence of the activation curves towards more

218 Because of the position of the voltage dependence of the available VSD structures, at p

219 ynamic simulations of KAT1, we show that the voltage dependence of the channel gate is highly sensiti

220 oupling, unitary current amplitudes, and the voltage dependence of the depolarization-induced activat

221 f the divalent strontium ion (Sr(2+)) on the voltage dependence of the G(V) curves of wild-type and c

222 Voltage dependence of the If activation curve and the in

223 ing in Kv1.2 channels and to investigate the voltage dependence of the initial binding of two Na(+) i

224 Here, we show that the voltage dependence of the inwardly rectifying potassium

225 that elastic load enhances positive shift of voltage dependence of the membrane capacitance because o

226 n which the depolarized state depends on the voltage dependence of the NMDA conductance at recurrent

227 The voltage dependence of the NV charge state can be used to

228 Single-channel recordings confirmed the voltage dependence of the penetration of chitohexaose mo

229 The bias voltage dependence of the phosphorescence, combined with

230 t border zone and this was attributed to the voltage dependence of the potassium channels.

231 However, the CAPOS mutation caused a weaker voltage dependence of the pumping rate and a stronger in

232 ed that it was fully active in modifying the voltage dependence of the rat skeletal muscle voltage-ga

233 tative modeling is still needed to study the voltage dependence of the relaxation process of synaptic

234 e domain, including the extension, rate, and voltage dependence of the S4 motion, as dictated by the

235 alization of lysine 41 in Cx26 increases the voltage dependence of the slow gate.

236 cal properties and bound to and modified the voltage dependence of the sodium channel Nav.

237 The voltage dependence of the sodium-dependent transient cur

238 Experiments to study the voltage dependence of the TcdA1 channel demonstrated tha

239 ch clamp experiments, we discovered a robust voltage dependence of the thromboxane receptor (TP recep

240 The voltage dependence of the VSD from Ci-VSP (Ci-VSD) is dr

241 ment (F161) do not significantly perturb the voltage dependence of the VSD movement, suggesting a uni

242 e hERG activation pathway, and that the weak voltage dependence of these transitions limits the overa

243 We investigated the voltage dependence of tonic currents in cultured rat hip

244 Examination of the voltage dependence of TRPA1 activation shows that sensit

245 ompanied by a slowly developing shift in the voltage dependence of TRPA1 towards more negative membra

246 ompanied by a slowly developing shift in the voltage dependence of TRPA1 towards more negative membra

247 hese modifications are due to a shift in the voltage dependence of TRPM8 activation toward more posit

248 neurons exhibit a depolarizing shift in the voltage dependence of TTX-S I(Na) inactivation, reduced

249 he role of permeating ions in generating the voltage dependence of unblock.

250 ur previous study, we found the kinetics and voltage dependence of voltage-sensor movements are very

251 Here, we show that the kinetics and voltage dependence of VSD movement in Ci-VSP can be tune

252 By comparing the voltage dependences of chemical modification and gating

253 We propose that the covariation of voltage dependences of ion channels represents a flexibl

254 fined protein, is supported by the lipid and voltage dependences of pore formation, and by molecular

255 igra pars compacta dopaminergic neurons, the voltage dependences of the A-type (I(A)) and H-type (I(H

256 ce expression and a hyperpolarizing shift in voltage-dependence of activation (gating).

257 ments revealed faster kinetics and shallower voltage-dependence of activation and deactivation for Ca

258 y, TEH1 caused hyperpolarizing shifts in the voltage-dependence of activation, fast inactivation and

259 caused a large hyperpolarizing shift in the voltage-dependence of activation, leading to substantial

260 ns in the allosteric site also abolished the voltage-dependence of agonist binding but did not reduce

261 in the orthosteric binding site underlie the voltage-dependence of agonist binding.

262 (2) receptor that may be responsible for the voltage-dependence of agonist binding.

263 Voltage-dependence of beta2-AR activation, however, was

264 ive patients, via a hyperpolarizing shift of voltage-dependence of both fast and slow inactivation an

265 tracellular pH significantly depolarized the voltage-dependence of both the QON/V and QOFF/V curves,

266 Near connections influence both voltage-dependence of C-type inactivation at the selecti

267 Low pH depolarizes the voltage-dependence of cardiac voltage-gated sodium (NaV1

268 O1 to the channels is complete, shifting the voltage-dependence of channel activation so that depolar

269 ntly modulate the BK channel by shifting its voltage-dependence of channel activation toward the hype

270 Comparison of the dynamics of voltage-dependence of clonidine- vs. norepinephrine-acti

271 The voltage-dependence of dielectric permittivity and the im

272 es except for a hyperpolarizing shift in the voltage-dependence of fast inactivation of DmNav26.

273 itivity depends on a pH-induced shift in the voltage-dependence of Ih activation that causes the open

274 DHF shifted voltage-dependence of INa availability by -3 mV compared

275 The voltage-dependence of inactivation was shifted in the hy

276 Voltage-dependence of Na(+)-coupled phosphate cotranspor

277 of mPanx1, and that the previously reported voltage-dependence of Panx1 channel gating is not direct

278 o combine the rapid kinetics and substantial voltage-dependence of rhodopsin family voltage-sensing d

279 ge-dependence of the charge movement and the voltage-dependence of the agonist binding.

280 e fluorescence signal and concomitantly, the voltage-dependence of the agonist binding.

281 A tight correlation was found between the voltage-dependence of the charge movement and the voltag

282 r alanine causes a considerable shift in the voltage-dependence of the cooperative transition(s) of B

283 4 did not modify either the amplitude or the voltage-dependence of the intramembrane charge movement.

284 We studied the voltage-dependence of voltage-sensor charge movement (QO

285 voltage-dependent, has smaller shifts in the voltage-dependences of conductance and steady-state inac

286 domains (VSDs) of K(+) channels to confer a voltage dependence on secretory traffic in parallel with

287 This mutation does not alter voltage dependence or kinetics of CaV2.1 currents, or fr

288 depolarizations by 64% without affecting its voltage-dependence or kinetics, and also caused a simila

289 Voltage dependence shifts affected channel kinetics by a

290 A735V shifted DII-VSD voltage dependence to depolarized potentials, whereas G7

291 ecelerated recovery and shifted inactivation voltage dependence to more negative potentials.

292 attenuates ERG inactivation by shifting its voltage dependence to more positive potentials, it enhan

293 dy we test the hypothesis that the channels' voltage dependences to a large extent are set by charged

294 This voltage dependence was blunted by electrogenic binding o

295 was not the case for PhTX-12 for which weak voltage dependence was observed.

296 This pattern of deadtime voltage dependence was repeated for all sources tested w

297 The range of voltage dependence was restricted by R295(7.40) in the a

298 rectifier K(+) current (IKr ) amplitude and voltage dependence were unaffected by high [Ca(2+) ]i .

299 tor-arrestin 3 interaction we determined the voltage-dependence with highest sensitivity in the physi

300 nt amino acids (444)EEEE abolishes intrinsic voltage dependence without altering the apparent Ca(2+)a