ライフサイエンスコーパス: voltage dependence

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

2 been attributed to fast kinetics and strong voltage dependence.

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

4 ent of EAG inactivation without altering its voltage dependence.

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

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

7 xchange transporters with varying degrees of voltage dependence.

8 vation kinetics and depolarized inactivation voltage dependence.

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

10 probability of nonlocal manipulation have a voltage dependence.

11 Cx26 equivalent region reduced the slow gate voltage dependence.

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

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

14 evealed dramatic alterations of kinetics and voltage dependence.

15 ed significant hyperpolarizing shifts in the voltage dependence.

16 selectivity, and only subtle differences in voltage dependence.

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

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

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

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

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

22 ts by inducing a leftward shift in the KCNQ3 voltage-dependence, a shift dependent on tryptophan 265.

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

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

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

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

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

28 The voltage dependence and fast kinetic components in the ac

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

30 to two distinct membranes is responsible for voltage dependence and inhibition of fusion.

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

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

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

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

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

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

37 units, required for the characteristic I(KS) voltage dependence and kinetics.

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

39 e negative shift ( approximately -140 mV) in voltage dependence and provides a molecular basis for ac

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

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

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

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

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

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

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

50 le heterooligomerization may also change the voltage-dependence and inactivation kinetics of the chan

51 2+) current, flattening of Ca(2+) transients voltage dependence, and enhanced frequency of spontaneou

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

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

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

61 nts indicate that S2 and S4 possess distinct voltage dependence, but functionally interact, such that

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 12-over-expressing myocytes manifest similar voltage dependence, current density and sensitivity to s

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

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

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

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

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

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

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

72 d for this because of the rapid kinetics and voltage dependence imparted to it by Mg(2+) ion block an

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

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

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

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

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 irectly senses membrane potential or whether voltage dependence is conferred indirectly.

82 The voltage dependence is enhanced at high extracellular Na(

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

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

91 ices, using the prepulse, were found to have voltage dependence nearly identical to that of currents

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

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

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

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

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

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

98 the human therapeutic range, normalizes the voltage dependence of activation and inactivation of thi

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

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

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

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

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

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

105 8 produce a marked shift in the BK channel's voltage dependence of activation in the hyperpolarizing

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

139 n constant of the blocker decreased, but the voltage dependence of block did not significantly change

140 Accordingly, reverse gradients shifted the voltage dependence of block, such that resurgent current

141 Voltage dependence of block, their important therapeutic

142 Thus, the voltage dependence of blocker unbinding results almost e

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

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

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

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

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

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

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

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

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

152 sm of how KCNE1 affects the VSD to alter the voltage dependence of channel activation, we perturbed t

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

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

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

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

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

158 It changes the voltage dependence of channel gating little.

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

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

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

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

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

164 The voltage dependence of cotransport and presteady-state ch

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

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

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

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

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

170 e distinct differences in their kinetics and voltage dependence of fast inactivation when expressed i

171 KCNQ1 channels exhibit indistinguishable voltage dependence of fluorescence and current signals,

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

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

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

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

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

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

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

179 There was no change in the voltage dependence of I(Ca) activation and inactivation.

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

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

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

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

184 , shows that mutant channels display altered voltage dependence of inactivation compared to wild type

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

186 ogue glutamic acid 1880 (K1826E) shifted the voltage dependence of inactivation toward that of Na(v)1

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

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

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

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

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

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

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

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

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

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

197 ein packing around S4, thereby affecting the voltage dependence of Kv7.1.

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

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

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

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

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

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

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

205 inear capacitance and positively shifted the voltage dependence of prestin, up to 120 mV, in cultured

206 The macroscopic voltage dependence of resurgent current raises the quest

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

208 The voltage dependence of SHG by four different probes, thre

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

210 a suggest that a hyperpolarized shift in the voltage dependence of sodium channel inactivation causes

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 In contrast, the voltage dependence of TASK3 channels is mediated through

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

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

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

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

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

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

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

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

233 A acts via a novel mechanism by reducing the voltage dependence of the sodium channel fast inactivati

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

235 The voltage dependence of the sodium-dependent transient cur

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

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

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

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

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

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

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

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

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

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

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

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

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

249 By comparing the voltage dependences of chemical modification and gating

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

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

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

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

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

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

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

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

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

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

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

261 The model further explained the voltage-dependence of block by PAP-1 and its thousand-fo

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

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

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

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

266 The mutation shifts the voltage-dependence of channel fast-inactivation in a dep

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

268 The voltage-dependence of dielectric permittivity and the im

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

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

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

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

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

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

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

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

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

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

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

280 ellular pH from 7.4 to 5.4 did not shift the voltage-dependence of the gating currents, but reducing

281 4 did not modify either the amplitude or the voltage-dependence of the intramembrane charge movement.

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

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

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

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

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

287 sistent with simple open-channel block, with voltage dependence reflecting interactions of the charge

288 Voltage dependence shifts affected channel kinetics by a

289 vation of Na(v)1.5 results in dose-dependent voltage dependence shifts of activation and inactivation

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

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

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

293 le somatic VGSCs activated with conventional voltage dependence (V(1/2) = -30 mV), they exhibited an

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 that the changes in maximal conductance and voltage dependence were not qualitatively affected by sp

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

298 current and large hyperpolarizing shifts of voltage dependence with graded shifts of half-activation

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