ライフサイエンスコーパス: voltage-dependent

1 ever, fentanyl-mediated block of I(hERG) was voltage dependent.

2 tizing current was amiloride insensitive and voltage dependent.

3 channels, the activation of which is steeply voltage-dependent.

4 m confirmed that this channel is malate- and voltage-dependent.

5 inii The EukCatB channels exhibit very rapid voltage-dependent activation and inactivation kinetics,

6 ion of peak transient Na(+) currents and the voltage-dependent activation and steady-state inactivati

7 -function) due to a hyperpolarizing shift of voltage-dependent activation combined with either decrea

8 perature by inducing a leftward shift in the voltage-dependent activation curve.

9 1 and the CaValpha2delta1-dependent shift in voltage-dependent activation gating.

10 In some K2P channels, strong voltage-dependent activation has been observed, but the

11 of Cav1.4FL, Cav1.4Deltaex 47 shows similar voltage-dependent activation in the presence and absence

12 tructural determinants that regulate CDI and voltage-dependent activation of Cav1.4, and is necessary

13 surface proteolytic cleavage of alpha2delta, voltage-dependent activation of channels is promoted, in

14 concentration, Rg3 shifted the half-point of voltage-dependent activation of currents by -14 mV for E

15 ong nonphysiological depolarization produces voltage-dependent activation of heterologously expressed

16 al hyperpolarization can be amplified by the voltage-dependent activation of Kir in neighboring cECs.

17 s processing is an essential step permitting voltage-dependent activation of plasma membrane N-type (

18 lytic processing of alpha2delta then permits voltage-dependent activation of the channels, acting as

19 n effects, including a depolarizing shift of voltage-dependent activation or a hyperpolarizing shift

20 f-function effects (hyperpolarizing shift of voltage-dependent activation, increased amplitude) in ni

21 increase in L-type current without altering voltage-dependent activation, thus reflecting an increas

22 Moreover, we show that the inhibition is voltage-dependent and competes with that by amiloride, a

23 nity of M2R for distinct ligands varies in a voltage-dependent and ligand-specific manner.

24 eraction, modulation of Cav2.2 was primarily voltage-dependent and transiently relieved by depolarizi

25 ngly enhanced by preincubation, was slightly voltage-dependent, and its washout was accelerated by bo

26 (3) Glycine directly bounded to voltage dependent anion channel 1 (VDAC1) on the mitocho

27 The voltage-dependent anion channel (VDAC) is the most abund

28 The voltage-dependent anion channel (VDAC) is the most abund

29 hort mtDNA fragments via pores formed by the voltage-dependent anion channel (VDAC) oligomers in the

30 A structure of the murine voltage-dependent anion channel (VDAC) was determined by

31 scription factor A (TFAM), citrate synthase, voltage-dependent anion channel (VDAC), and cytochrome c

32 ally occurring nanopore of the mitochondrial voltage-dependent anion channel (VDAC), reconstituted in

33 nine nucleotide translocase (ANT) and of the voltage-dependent anion channel (VDAC).

34 chondrial fission factor (MFF1 and MFF2) and voltage-dependent anion channel (VDAC1) as a novel regul

35 The voltage-dependent anion channel 1 (VDAC-1) is an importa

36 rated that mitochondrial calcium released by voltage-dependent anion channel 1 (VDAC1) after sciatic

37 hemical mitophagy inducer, overexpression of voltage-dependent anion channel 1 (VDAC1) induced Parkin

38 The outer mitochondrial membrane protein voltage-dependent anion channel 1 (VDAC1) is a convergen

39 by gene ontology analysis, the expression of voltage-dependent anion channel 1 (VDAC1), a constituent

40 e outer-mitochondrial membrane (OMM) protein voltage-dependent anion channel 1 (VDAC1).

41 r and inner mitochondrial membrane channels, voltage-dependent anion channel 1 and the mitochondrial

42 acromolecular complex composed of the VDAC1 (voltage-dependent anion channel 1), the GRP75 (chaperone

43 We further discover the mitochondrial porin voltage-dependent anion channel 2 (VDAC2) as essential c

44 TPR3 binds to voltage-dependent anion channel 3, but although this is

45 el membrane proteins, including the abundant voltage-dependent anion channel and the cation-preferrin

46 Here, using the human voltage-dependent anion channel as our template scaffold

47 structurally different beta-barrel channels: voltage-dependent anion channel from outer mitochondrial

48 consumption, mitochondrial DNA content, and voltage-dependent anion channel protein expression.

49 As expected, TcMCU was co-localized with the voltage-dependent anion channel to the mitochondria.

50 of our neurosteroid ligand in the IMP, mouse voltage-dependent anion channel-1 (mVDAC1), and top-down

51 by activating a conductive pathway involving voltage-dependent anion channel-1 (VDAC-1) and by exocyt

52 reatment of HBE cells with inhibitors of the voltage-dependent anion channel-1 (VDAC-1) or treatment

53 n corneal epithelia, INSR interacts with the voltage-dependent anion channel-1 (VDAC1) in mitochondri

54 Voltage-dependent anion channel-1 (VDAC1) is a highly re

55 ns, the most abundant OMM transporter is the voltage-dependent anion channel.

56 The voltage-dependent anion channels (VDAC) were identified

57 vatable ceramide probe, we here identify the voltage-dependent anion channels VDAC1 and VDAC2 as mito

58 Erastin, the ferroptosis activator, binds to voltage-dependent anion channels VDAC2 and VDCA3, but tr

59 The oligomeric organization of the voltage-dependent anion-selective channel (VDAC) and its

60 lusters of mitochondrial proteins, including voltage-dependent anion-selective channels, were also im

61 We observed voltage-dependent asymmetric distortions of the VDAC-1 b

62 iquitin-mediated degradation of calcium- and voltage-dependent big potassium (BK) channels.

63 l(-) channel (CaCC), is activated by direct, voltage-dependent, binding of intracellular Ca(2+) .

64 K(2P) channels, which results in an unusual voltage-dependent block of leak channels belonging to th

65 ) ) entry into pancreatic beta-cells through voltage-dependent Ca(2+) (Ca(V) ) channels.

66 localize and form ion channel complexes with voltage-dependent Ca(2+) (CaV) channels.

67 Retigabine inhibited voltage-dependent Ca(2+) channel (VDCC) currents and red

68 ransiently increase expression of the T-type voltage-dependent Ca(2+) channel (VDCC) subunit Ca(V)3.2

69 ctional beta-cell mass determination through voltage-dependent Ca(2+) channel (VDCC)-mediated interna

70 e thought to act as allosteric modulators of voltage-dependent Ca(2+) channel activation, whereas phe

71 Voltage-dependent Ca(2+) channel activity is dependent o

72 rticosterone (11-DHC) and cortisone suppress voltage-dependent Ca(2+) channel function and Ca(2+) flu

73 Egr1 to regulate also the expression of the voltage-dependent Ca(2+) channel subunit alpha2delta4, w

74 ion through a direct interaction with L-type voltage-dependent Ca(2+) channels (Ca(V) 1.2 and Ca(V) 1

75 -gated Na(+) channels (Nav) and subsequently voltage-dependent Ca(2+) channels (Cav).

76 rolox and to nifedipine, a blocker of L-type voltage-dependent Ca(2+) channels (LVDCCs).

77 [Ca(2+)] spikes, which depend on the L-type voltage-dependent Ca(2+) channels (VDCCs) and require ac

78 hibitors of BDNF-TrkB signaling or of L-type voltage-dependent Ca(2+) channels (VDCCs) block the anti

79 lation of ryanodine receptors (RyRs), L-type voltage-dependent Ca(2+) channels (VDCCs) or TMEM16A Ca(

80 strointestinal muscles are important because voltage-dependent Ca(2+) channels in smooth muscle cells

81 els are positioned in clusters away from the voltage-dependent Ca(2+) channels that mediate glutamate

82 eptor potential channels, the P2X receptors, voltage-dependent Ca(2+) channels, and the inositol 1,4,

83 structure dissimilarity to known ligands for voltage-dependent Ca(2+) channels, selective binding aff

84 brane, Ca(2+) entry primarily occurs through voltage-dependent Ca(2+) channels.

85 During a triggered AP, a voltage-dependent Ca(2+) conductance was fractionally ac

86 1 reduced K(+)-induced insulin secretion and voltage-dependent Ca(2+) currents.

87 TOCs) that hyperpolarize the cell and reduce voltage-dependent Ca(2+) entry.

88 Intravascular pressure activates voltage-dependent Ca(2+) influx that stimulates the retu

89 t hyperpolarize the cell membrane and reduce voltage-dependent Ca(2+) influx.

90 charged amino acids at the inner pore and a voltage-dependent Ca(2+)/Mg(2+) block.

91 Two candidate modules featuring voltage-dependent Ca2+-channels link these outputs to th

92 ial due to the opening of NMDA receptors and voltage dependent calcium channels.

93 Voltage-dependent calcium (Ca(V)) 1.3 channels are invol

94 TMEM16A is opened by voltage-dependent calcium binding and regulated by perme

95 el invokes the modulation of CaV2.3 (R-type) voltage-dependent calcium channel (VDCC) currents observ

96 NNK induces voltage-dependent calcium channel (VDCC)-intervened calc

97 n, the metabotropic glutamate receptor 6 and voltage-dependent calcium channel alpha1.4, are not dete

98 The authors identify two proteins, the voltage-dependent calcium channel auxiliary subunit BARP

99 Voltage-dependent calcium channels (Cav) of the T-type f

100 This limits calcium influx through voltage-dependent calcium channels and dampens adrenergi

101 teins (Cacna2d1-4) are auxiliary subunits of voltage-dependent calcium channels that also drive synap

102 gh inhibition of K(ATP) channels, opening of voltage-dependent calcium channels, increased [Ca(2+)](i

103 BARP, an auxiliary subunit of voltage-dependent calcium channels, promoted alpha6beta4

104 to membrane depolarization and activation of voltage-dependent calcium channels, resulting in calcium

105 these effects are dependent on activation of voltage-dependent calcium channels.

106 cardiac excitation-contraction coupling and voltage-dependent calcium channels.

107 orters, GABA-A receptors and regulators, and voltage-dependent calcium channels.

108 Gating of voltage-dependent cation channels involves three general

109 harge-like bursting by gating a nonselective voltage-dependent cationic current.

110 Voltage-dependent CaV1.2 L-type Ca(2+) channels (LTCC) a

111 of neutrons allowed the determination of the voltage-dependent changes in both the profile structure

112 Amplitude changes scaled with voltage-dependent changes in membrane input resistance.

113 We show that voltage-dependent changes in membrane resistance amplify

114 intrinsic membrane properties often indicate voltage-dependent changes in membrane resistance and tim

115 confocal microscopy, we demonstrate that the voltage-dependent changes in the membrane tension induce

116 452A nearly eliminated the effects of Rg3 on voltage-dependent channel gating but did not prevent the

117 elated potassium channel (hERG, Kv11.1) is a voltage-dependent channel known for its role in repolari

118 everely distorted measurements and recruited voltage-dependent channels.

119 More importantly, the voltage-dependent characteristics of Ln(3+)'s action led

120 We also note that the occurrence of voltage-dependent charge movements in other SLC26 family

121 potassium cation efflux antiporter KEA3 and voltage-dependent chloride channel VCCN1 and suggest tha

122 udied the effects of non-Markovian power-law voltage dependent conductances on the generation of acti

123 c transmission and is shaped by a variety of voltage-dependent conductances.

124 gnal via the influx of calcium ion (Ca(2+)), voltage-dependent conformational change (VDeltaC), or a

125 state and a depolarized state resulting from voltage-dependent conformational changes during a 10-mus

126 site-specific fluorescent labeling to track voltage-dependent conformational changes similar to cyst

127 compared, probably undergo rather different voltage-dependent conformational changes when they open.

128 ants were blocked, but Na(+) binding and the voltage-dependent conformational transitions were unaffe

129 his phenomenon depends on the recruitment of voltage-dependent currents (e.g., NMDAR-mediated Ca(2+)

130 Neuronal subthreshold voltage-dependent currents determine membrane properties

131 PICs are intrinsic, voltage-dependent currents that activate strongly when m

132 harge transport through DNA and the strongly voltage-dependent currents that are measured through org

133 L-type Ca(2+) channels terminates because of voltage-dependent deactivation and not by Ca(2+)-depende

134 synapses between Cx36-KO neurons had faster voltage-dependent decay kinetics and conductance asymmet

135 on arises not from the downstream effects of voltage-dependent drug uptake, but rather directly from

136 minoglycoside activity, which is ascribed to voltage-dependent drug uptake.

137 AD(P)H fluorescence signal and low uptake of voltage-dependent dyes, but are energized by a pH gradie

138 ion acts to refill those stores by promoting voltage-dependent entry of extracellular calcium.

139 ncrease with temperature, the conformational voltage-dependent equilibria are virtually insensitive t

140 sium ('SK') channels, and longer-lasting and voltage-dependent excitation involving non-specific cati

141 sium ('SK') channels, and longer-lasting and voltage-dependent excitation involving non-specific cati

142 acidification-induced uncoupling, absence of voltage-dependent fast inactivation, longer channel open

143 uorometry measurements were performed with a voltage-dependent fluorophore/quencher pair.

144 PhTX-343 inhibition was strongly voltage-dependent for all subunit combinations except al

145 acceleration of electrochemical reactions by voltage-dependent formation of the interfacial microreac

146 networks by delaying inactivation of axonal voltage-dependent [Formula: see text] channels, this mec

147 and Ni(2+) Also absent was the capacity for voltage-dependent G-protein inhibition by co-expressed T

148 We conclude that voltage-dependent gating and pore opening in BK channels

149 between the PAS, CNBHD, and VS that modulate voltage-dependent gating and provide evidence that VS mo

150 ressed whether these two major mechanisms of voltage-dependent gating are conserved in K(V)10.2 chann

151 1 intracellular domains are not required for voltage-dependent gating but likely interact with the VS

152 esidues are important for H(+) transport and voltage-dependent gating in the CLC exchangers.

153 between the three domains affects cAMP- and voltage-dependent gating in three HCN isoforms.

154 Here, we show voltage-dependent gating is common to most K2P channels

155 llular ATP, respectively, as cofactors, thus voltage-dependent gating is dependent on multiple stimul

156 t results from a unique combination of steep voltage-dependent gating kinetics and ultra-fast voltage

157 tructure of the resting state and a complete voltage-dependent gating mechanism.

158 y studied, the detailed structural basis for voltage-dependent gating mechanisms remain obscure.

159 Connexin-based channels exhibit two distinct voltage-dependent gating mechanisms termed slow and fast

160 n peak current density and modulation of the voltage-dependent gating of CaV1.2.

161 ted increase in the peak current density and voltage-dependent gating of CaV1.2.

162 The physical mechanism underlying the voltage-dependent gating of K channels is usually addres

163 report a two-stage E-M coupling mechanism in voltage-dependent gating of K(V)7.1 as triggered by VSD

164 ins likely play a similar modulatory role in voltage-dependent gating of the related K(v)11-12 channe

165 structure, suggesting that the mechanism of voltage-dependent gating of these two channels is quite

166 g ion channel models with single exponential voltage-dependent gating variable rate constants, parame

167 of iPSC-CMs, composed of single exponential voltage-dependent gating variable rate constants, parame

168 o interact with S4-S5(L) to modulate channel voltage-dependent gating, as N-Cap deletion drastically

169 etermine the effects of mutations on channel voltage-dependent gating.

170 novel insights on fundamental principles of voltage-dependent gating.

171 d, which suggest an alternative mechanism of voltage-dependent gating.

172 act to modulate Ca(2+)-calmodulin as well as voltage-dependent gating.

173 orters, we show that the lack of uniport and voltage-dependent H(+) /Cl(-) symport originate from str

174 ylthiophene) electrochemical devices exhibit voltage-dependent heterogeneous swelling consistent with

175 sic decay, the rate of which was only weakly voltage dependent, in contrast to that in previously cha

176 mutation also caused an opposite increase in voltage-dependent inactivation (VDI), resulting in a mul

177 alent, as they produce comparable defects in voltage-dependent inactivation and cause similar manifes

178 ically, the TS2 mutation reduced the rate of voltage-dependent inactivation and shifted leftward the

179 es the amplitude of the action potentials by voltage-dependent inactivation of the Na(+) channels inv

180 ations in nCa(V) confer unusually sensitive, voltage-dependent inactivation to inhibit responses to n

181 ta2X13-containing channels exhibited greater voltage-dependent inactivation.

182 n of Ca(V) 1.2 and accelerates recovery from voltage-dependent inactivation; TSPAN-7 also slows Ca(V)

183 In stellate cells, a voltage-dependent increase in membrane resistance at sub

184 I(SK) rectification by reducing the Ca(2+) /voltage-dependent inhibition of SK channels without chan

185 rectification of I(SK) via reduction Ca(2+) /voltage-dependent inhibition of the channels at high [Ca

186 ingly, this effect of HX531 occurred through voltage-dependent inhibition of VGCCs, a phenomenon know

187 ted I (Ca) but produced G protein-dependent, voltage-dependent inhibition of VGCCs.

188 Nonetheless, neurons express voltage-dependent intrinsic properties that can potentia

189 (2) elicited a prolonged, concentration- and voltage-dependent inward current, associated with an inc

190 Results Experiments revealed tube voltage-dependent iodine attenuation curves, which were

191 canonical VSD-pore coupling, are at work in voltage-dependent ion channel activation.

192 These temperature-dependent changes in voltage-dependent ion channel kinetics (rates of opening

193 ntial [1], ionic gradients across cells [2], voltage-dependent ion channels [3], molecular motors [4-

194 ructural module that regulates the gating of voltage-dependent ion channels in response to a change i

195 losing of the central ion-conducting pore in voltage-dependent ion channels is gated by changes in me

196 tivation is an intrinsic property of several voltage-dependent ion channels, closing the conduction p

197 ance, filtering of the receptor potential by voltage-dependent ion channels, is ubiquitous in all non

198 largely shaped by different combinations of voltage-dependent ion channels.

199 function of cooperative interactions between voltage-dependent ionic channels remains largely unknown

200 m that can act in parallel with other purely voltage-dependent ionic mechanisms for EAD initiation.

201 and large-conductance, Ca(2+)-activated, and voltage dependent K(+) (BK) channels.

202 4-aminopyridine or related voltage-dependent K channel blockers could be a useful a

203 actory information by decreasing activity of voltage-dependent K channels (Kv1.3).

204 ype Ca(2+) channels, K(ATP) (Kir6) channels, voltage-dependent K channels (Kv4, Kv7, and Kv11), twin-

205 essed large-conductance Ca(2+)-activated and voltage-dependent K(+) (BK) channels, critical for mucoc

206 Ca(2+)- and voltage-dependent K(+) (BK) currents and the expression

207 KEY POINTS: Several different voltage-dependent K(+) (KV ) channel isoforms are expres

208 ance-size arteries express several different voltage-dependent K(+) (KV ) channels, including KV 1.5

209 study, we examine the mechanism by which the voltage-dependent K(+) (Kv) channel Kv2.1 (KCNB1) facili

210 ontrols the membrane expression of the human voltage-dependent K(+) channel human ether-a-go-go-relat

211 KCNQ1, also known as Kv7.1, is a voltage-dependent K(+) channel that regulates gastric ac

212 STRACT: Large-conductance KCa (BK) and other voltage-dependent K(+) channels (Kv) are highly expresse

213 ance Ca(2+) -activated K(+) channel (BK) and voltage-dependent K(+) channels (Kv) on [Ca(2+) ]i respo

214 K(V) 7 channels are a family of voltage-dependent K(+) channels expressed in many cell t

215 K(V) 7 channels are voltage-dependent K(+) channels that open in response to

216 tivator retigabine (10 muM) had no effect on voltage-dependent K(+) currents or resting membrane pote

217 titration technique (GITT) analysis provides voltage-dependent K(+) diffusion coefficients that range

218 Our data suggest that voltage-dependent K+ channel inhibition with 4-aminopyri

219 re larger in external Ba(2+) than in Ca(2+); voltage-dependent kinetics of activation, inactivation,

220 nerative disease induced by mutations in the voltage-dependent Kv3.3 potassium channel.

221 a hormone known to modulate the activity of voltage-dependent L- and T-type Ca(2+) channels that are

222 The voltage-dependent L-type Ca(2+) channel was identified a

223 d Cl(-) channels (ANO1, encoded by Ano1) and voltage-dependent L-type Ca(2+) channels (CavL , encoded

224 tivated Cl(-) channels (encoded by Ano1) and voltage-dependent L-type Ca(2+) channels (encoded by Cac

225 Voltage-dependent L-type Ca(V) 1.2 channels play an indi

226 Calcium influx through the voltage-dependent L-type calcium channel (CaV1.2) rapidl

227 ated by increased intracellular calcium in a voltage-dependent manner but, unlike many other TRP chan

228 s), through which ions and ATP permeate in a voltage-dependent manner to control neuronal excitabilit

229 ABSTRACT: Ca(2+) sparks are generated in a voltage-dependent manner to initiate spontaneous transie

230 Ca(2+) sparks are generated in a voltage-dependent manner to initiate spontaneous transie

231 2(Q) homomeric receptors in an activity- and voltage-dependent manner, indicating a pore block mechan

232 NMDA receptor currents in a dose-, pH-, and voltage-dependent manner.

233 presequence peptide in a concentration- and voltage-dependent manner.

234 No voltage-dependent mechanism that synchronized Ca(2+) tra

235 at thalamocortical neurons have postsynaptic voltage-dependent mechanisms that can amplify integrated

236 ansporter 12 (ALMT12) is a malate-activated, voltage-dependent member of the aluminum-activated malat

237 consideration for the role of non-linear and voltage-dependent membrane properties.

238 potential to these deformations based on the voltage-dependent membrane tension-the mechanism observe

239 Ketamine, a non-competitive, voltage-dependent N-Methyl-D-aspartate receptor (NMDAR)

240 In this study, we showed that voltage-dependent Na(+) currents are regulated in a slow

241 ll explained by a tetrodotoxin-sensitive and voltage-dependent Na(+) persistent inward current (NaPIC

242 n of the myocardium, which causes a block of voltage-dependent Na+ channels throughout the myocardial

243 -dependent CatSper dynamics articulated with voltage-dependent neutral sodium-proton exchanger (NHE).

244 that decay in approximately 1 ms and mildly voltage-dependent NMDA receptor EPSCs of approximately 0

245 al changes that likely prime the channel for voltage-dependent opening.

246 ing has to be considered together with other voltage-dependent partial reactions to cooperatively det

247 ctions of GABA operate in parallel to effect voltage-dependent pH changes, a novel mechanism for regu

248 Voltage-dependent potassium (K(v)) channels play a funda

249 The voltage-dependent potassium (Kv) channel Kv1.3 regulates

250 ents nerve injury-induced methylation of the voltage-dependent potassium (Kv) channel subunit Kcna2 p

251 ood flow responses, and identify upregulated voltage-dependent potassium channel (KV) number in cereb

252 The voltage-dependent potassium channel Kv1.3 plays essentia

253 nd that reduced functional expression of the voltage-dependent potassium channel subunit Kv1.1 substa

254 The voltage-dependent potassium channel subunit Kv3.3 is exp

255 Voltage-dependent potassium channels (K(v)s) gate in res

256 Changes in voltage-dependent potassium channels (Kv channels) assoc

257 elopmental transcriptional regulation of Kv1 voltage-dependent potassium channels and the resulting p

258 that METH exposure affected the activity of voltage-dependent potassium channels in these neurons.

259 Voltage-gated Kv7 (KCNQ) channels are voltage-dependent potassium channels that are activated

260 Smooth muscle cells express Kv7.4 and Kv7.5 voltage-dependent potassium channels, which have each be

261 ic compartment, and 2) reduced activation of voltage-dependent potassium channels.

262 nit KCNQ1 to generate the slowly activating, voltage-dependent potassium current (IKs) in the heart t

263 ed at the axonal plasma membrane where their voltage-dependent potassium currents suppress neuronal e

264 These channels exhibit a behavior called voltage-dependent potentiation (VDP), which appears to b

265 atch-clamping allows ion transport and other voltage-dependent processes to be studied while controll

266 erized by a unique time- and transjunctional voltage-dependent profile, we investigated whether the e

267 These findings aligned with the voltage-dependent profiles of L- and T-type Ca(2+) chann

268 These voltage-dependent protein changes include asymmetric bar

269 and validate the method on two prototypical voltage-dependent proteins, the Kv1.2 K(+) channel and t

270 We demonstrate that the voltage-dependent rate at which a membrane-embedded VDAC

271 hus, the alanine residue Ala(254) determines voltage-dependent rectification upon receptor desensitiz

272 ellular stores, mAChR activation facilitates voltage-dependent refilling of calcium stores, thereby m

273 Extending our study into the nonlinear, voltage-dependent regime, we increased stimulus amplitud

274 ic reticulum luminal Ca(2+), and Ca(2+)- and voltage-dependent regulation of RyR1-G4941K mutant chann

275 crease resurgent currents, which involve the voltage-dependent release of an open channel blocker.

276 From the gate voltage-dependent response, we extract the binding const

277 Irregular voltage-dependent single-channel currents, high gating c

278 The voltage-dependent SLAC1 transporters do not use proton o

279 has no charge in this region, still presents voltage-dependent slow gating suggests that charges stil

280 lyses mapped SpMae1(p) and AcDct(p) into the voltage-dependent slow-anion channel transporter (SLAC1)

281 Voltage-dependent sodium (Na(V)) 1.8 channels regulate a

282 Voltage-dependent sodium and calcium channels in pain-in

283 ated by a nonlinear dynamical interaction of voltage-dependent sodium and fast-inactivating potassium

284 Mutations in voltage-dependent sodium channels cause severe autism/in

285 osamide is an antiseizure agent that targets voltage-dependent sodium channels.

286 rrent (INaP), a non-inactivating mode of the voltage-dependent sodium current, paradoxically increase

287 We show that this discrepancy is due to a voltage-dependent spike-synchronization mechanism inhere

288 mory are governed by two implicitly-coupled, voltage-dependent state variables-membrane radius and th

289 In rare cases, rapid, voltage-dependent stochastic switching is observed, cons

290 of Nav1.4 with the bound toxins, and reveal voltage-dependent structural changes related to channel

291 teric regulation of open probability through voltage-dependent subunit activation is thought to prece

292 ion potential can exhibit distinct time- and voltage-dependent thresholds, and also demonstrating tha

293 gical model of repolarization similar to the voltage dependent, time-independent rectifying outward p

294 Ca(2+) channels and mediated by Ca(2+)- and voltage-dependent transient receptor potential melastati

295 p the determinants of S4 helix motion during voltage-dependent transition from the intermediate to th

296 duced a deeper closed state through a weakly voltage-dependent transition.

297 Moreover, Kv1.3 voltage-dependent transitions from closed to open confor

298 gical measurements showing a decrease in the voltage-dependent transmembrane ionic currents after pul

299 In summary, our work highlights that the voltage-dependent triggering of Ca(2+) sparks/STOCs is n

300 a thin insulating gap, we examine the local voltage-dependent variation of potential barrier height