ライフサイエンスコーパス: channel opening

1 which the membrane deformation changes upon channel opening.

2 ires a match between agonist binding and ion channel opening.

3 olecular coupling between ligand binding and channel opening.

4 effects of GV-58 to be dependent upon Ca(2+) channel opening.

5 oltage and temperature sensor activation and channel opening.

6 bsequently binds to TRPC1 subunits to induce channel opening.

7 bundle of intracellular loops (ICLs) during channel opening.

8 main acts as a coupling domain for efficient channel opening.

9 nt for enabling the late cooperative step of channel opening.

10 VSD IV did not appear to participate in channel opening.

11 turn, with a diameter of 25A of the central channel opening.

12 nucleotide-binding domain (CNBD) facilitates channel opening.

13 oltage dependent and closely correlates with channel opening.

14 lular ligand is coupled to the transmembrane channel opening.

15 (Ala-621) below the gate is responsible for channel opening.

16 as a result of the longer duration of IP(3)R channel opening.

17 modulation of ligand binding and subsequent channel opening.

18 ct both the second conformational change and channel opening.

19 the manner by which agonist binding leads to channel opening.

20 en proposed to transduce Ca(2+) binding into channel opening.

21 ntry within the dendritic spine that follows channel opening.

22 d Orai1 from binding to STIM1 and subsequent channel opening.

23 domain around the ligand, culminating in ion channel opening.

24 tal binding to a pair of histidines promoted channel opening.

25 e negatively charged residues, thus favoring channel opening.

26 hed conformational changes necessary for ion channel opening.

27 side the intracellular vestibule, precluding channel opening.

28 nct sites, voltage sensor activation, and BK channel opening.

29 agonist binding, receptor preactivation, and channel opening.

30 ements following ligand binding resulting in channel opening.

31 closing at substantially lower tensions than channel opening.

32 at transfer the energy of agonist binding to channel opening.

33 moving "down" (toward the cytoplasm) during channel opening.

34 ing force for release upon ER Ca(2+) release channel opening.

35 vely-charged Glu did not induce constitutive channel opening.

36 ng GluN1 gating movements immediately before channel opening.

37 cessary and sufficient for TRIP8b to inhibit channel opening.

38 onal changes that then trigger regulation of channel opening.

39 multiple voltage sensors before KCNQ1/KCNE1 channel opening.

40 losteric coupling between Ca(2+) binding and channel opening.

41 herefore crucial to couple ligand binding to channel opening.

42 tionship between voltage sensor movement and channel opening.

43 e sensor movements and their relation to ion channel opening.

44 more effective in coupling Ca(2+) binding to channel opening.

45 separation remains as the driving force for channel opening.

46 inding between His of both monomers inhibits channel opening.

47 ment of TRPV1 pore turret that is coupled to channel opening.

48 and determine the iris-like mechanism of ion channel opening.

49 e and active states but is not essential for channel opening.

50 slated to the transmembrane domain, inducing channel opening.

51 f regions of TRPC1 implicated in controlling channel opening.

52 ting AChR, decreasing the probability of ion channel opening.

53 required unusually large depolarizations for channel opening.

54 and synchronizes initial ligand binding with channel opening.

55 s major structural rearrangements leading to channel opening.

56 ls a second phase of CAD/STIM1 binding after channel opening.

57 ortant role in coupling of ligand binding to channel opening.

58 ng rearrangements that are necessary for ion channel opening.

59 lular [Ca(2+)], which is indicative of P2X7R channel opening.

60 lix to the plasma membrane potentiates CNGA1 channel opening.

61 ains (NBDs), preventing NBD dimerization and channel opening.

62 can act normally or tangentially to the ring channel opening.

63 s for the kinetics and localization of Orai1 channel opening.

64 +) , acting through calmodulin to facilitate channel opening.

65 hysical mechanisms of Ca(2+) selectivity and channel opening.

66 d LBD, on much longer timescales compared to channel opening.

67 stsynaptic processes occurring after GABAA-R channel opening.

68 which TRPV1 translates diverse stimuli into channel opening.

69 itions substantially inhibited ATP-dependent channel opening.

70 K also diminished noticeably the duration of channel openings.

71 , it significantly enhanced the frequency of channel openings.

72 1(F246S) mutations also produced spontaneous channel openings.

73 levels of free Zn(2+) were found to inhibit channel openings.

74 -68 or Lys-170 markedly slow the kinetics of channel opening (500 and 700 ms for W68L and K170N, resp

75 higher concentration of GABA for detectable channel openings, a major population of brief openings,

76 underlying these observations is a delay in channel opening after application of protons, most likel

77 ease of the Glu167/Arg290 salt bridge during channel opening allows a strong ionic interaction betwee

78 Channel opening allows signal sequence insertion into a

79 hole-cell recording, we measured the rate of channel opening, among other kinetic properties, for a s

80 on of TRIP8b with HCN subunits both inhibits channel opening and alters channel membrane trafficking,

81 'head-tail' interaction, thereby suppressing channel opening and attenuating IP3R-mediated Ca(2+) rel

82 motaxis that link receptor activation to TRP channel opening and Ca2+ signaling.

83 e and the equilibrium constants pertinent to channel opening and channel desensitization for this mut

84 Ion channel opening and closing are fundamental to cellular

85 Our experimental results suggest that both channel opening and closing are initiated by the transme

86 In contrast, sole modification of anion channel opening and closing is insufficient to account f

87 nnels that we infer allow us to propose that channel opening and closing may be associated with a rel

88 esults indicate a more dynamically regulated channel opening and closing than previously thought and

89 or suggesting functional properties such as channel opening and closing upon ligand binding, pH-indu

90 Channel opening and closing were altered by mutations in

91 Channel opening and closing were observed in simulations

92 unanswered questions about the mechanism of channel opening and closing, the location and nature of

93 ion and decay kinetics match the kinetics of channel opening and closing.

94 cles of sodium channels and the mechanism of channel opening and closing.

95 e lateral plane contributed cooperatively to channel opening and closing.

96 in animal Shaker-like channels that lead to channel opening and closing.

97 of conformational rearrangements during ion channel opening and closing.

98 om the ATP-dependent mechanism that controls channel opening and closing.

99 the channel pore have been described during channel opening and closing; however, the relative impor

100 GluA2R flop isoform accelerates the rate of channel opening and desensitization for GluA1/2R channel

101 ing and the conformational changes governing channel opening and desensitization remain unknown.

102 hypothesis that there are separate gates for channel opening and desensitization.

103 show how the permeation pathway changes upon channel opening and identify conformational changes thro

104 sumption accompanied by spontaneous GABA ion channel opening and increased accumbal tonic current.

105 The mutation causes spontaneous GABA ion channel opening and increases GABA sensitivity of recomb

106 ents calcium current density by facilitating channel opening and increasing the number of channels in

107 Trp-68 and Lys-170) that control the rate of channel opening and inhibition in response to ATP.

108 Current inhibition requires channel opening and is strongly voltage dependent, being

109 ed (HCN) channel by simultaneously recording channel opening and ligand binding, using the patch-clam

110 ne helps set the energy barrier to both CFTR channel opening and MRP-mediated drug efflux and that CF

111 of the Asp-96 homolog is required for cation channel opening and occurs >10-fold faster than reproton

112 ly a result of a decreased likelihood of the channel opening and remaining open.

113 ization of intracellular K(+) depletion upon channel opening and restoration of cytoplasmic K(+) afte

114 arly markedly prolongs the lag that precedes channel opening and slows the subsequent rise of K(+) cu

115 t BK gating mechanisms converge to determine channel opening and that these gating mechanisms are all

116 implies that voltage control of both Ca(2+) channel opening and the driving force for Ca(2+) entry a

117 ting with Calmodulin and responsible for the channel opening and the K(+) efflux.

118 her valine or proline, the former preventing channel opening and the latter modifying both ion transl

119 rs upon sustained membrane depolarization or channel opening and then recovers during hyperpolarized

120 e to apparent one-to-one coupling between Ca channel opening and vesicle release, allowing presynapti

121 zing shift in the voltage dependence of both channel opening and VSD activation, reported by a fluoro

122 arization, suggesting that the rates of hERG channel opening and, critically, that of deactivation mi

123 ning native Aplysia Slack channels increased channel opening and, in current-clamp recordings, produc

124 s ability to increase the duration of longer channel openings and their frequency, resulting in longe

125 At mouse body temperature, the channel-opening and -closing rate constants are approxim

126 f, by measuring its inhibitory effect on the channel-opening and channel-closing rate constants as we

127 as enzymes clamping onto substrates, and ion channels opening and closing.

128 coiled-coil domain couples inactivation with channel opening, and is enabled by negatively charged re

129 alpain-1 activation following T-type calcium channel opening, and resulted in the truncation of a reg

130 ates the coupling between Ca(2+) binding and channel opening, and, although sharing structural homolo

131 rE, it remains unclear how drug delivery and channel opening are connected.

132 wever, the transitions in TM2 that accompany channel opening are incompletely understood and remain u

133 ns on the involvement of glutamic acid 90 in channel opening are ruled out by demonstrating that E90

134 icient (Q(10)) of approximately 40], and the channel openings are accompanied by large changes in ent

135 )-sensitive, large-conductance K(+) (BK(Ca)) channel opening as iberiotoxin (100 nM) significantly re

136 oves at the protein-lipid interface to drive channel opening, as the target for these amphipathic neu

137 ivation at 33-39 degrees C and achieved full channel opening at 42 degrees C.

138 ally completed within 2 ms and occur without channel opening at low proton concentration, indicating

139 ts in its voltage activation curve, allowing channel opening at physiological membrane potentials.

140 significantly greater potency, inducing full channel openings at lower (fM) toxin concentrations wher

141 of activation, increasing the probability of channel openings at physiological membrane potentials.

142 me resolution of the inherently brief alpha7 channel openings, background mutations or a potentiator

143 individual voltage-sensor movements lead to channel opening before all voltage sensors have moved.

144 the rate or the equilibrium constants of the channel opening but does slow down the channel desensiti

145 ivity of voltage activation, specifically of channel opening, but not channel closing, which is remin

146 nist of the NMDAR that is required for NMDAR channel opening, but which cannot mediate neurotransmiss

147 th His(950) of cytoplasmic loop 3 to prevent channel opening by ATP in the non-phosphorylated state a

148 Channel opening by Ca(2+) is made possible by a structur

149 ation of these residues to alanines promoted channel opening by curcumin in an ATP-dependent manner e

150 We found that NGF reduces Maxi-K channel opening by decreasing the activity of nifedipine

151 Allosteric control of Hv1 channel opening by DeltapH (V-DeltapH coupling) is manif

152 vide a potential mechanism for inhibition of channel opening by F508del and support the dimer interfa

153 f ASIC3, previously shown to be critical for channel opening by GMQ, disrupted the GMQ effects on ina

154 hate (PIP2) or clotrimazole is necessary for channel opening by PS.

155 with HpTx2 increases the energy barrier for channel opening by slowing activation and accelerating d

156 However, postsynaptic TRPC channel opening by the PI3K-PLC signalling pathway in PO

157 ial motion of the pore-lining helices effect channel opening by widening the pore asymmetrically and

158 function, we investigated the regulation of channel openings by intracellular pH.

159 closed and three open states, and shows that channel opening can occur from partially liganded states

160 ts numerous biophysical properties including channel opening, closing, and inactivation.

161 atalytic acid base Lys(295), suggesting that channel opening/closing motions of the Glu are synchroni

162 can provide insights into the mechanisms of channel opening complementing those from the structural

163 eceptor channels (AChRs) to promote a global channel-opening conformational change.

164 in single channel recordings; more frequent channel openings correlates with the degree of antibody

165 Short-latency Ca(2)(+) channel opening coupled to multivesicular release would

166 ubunit confers nearly maximal suppression of channel opening, despite four binding sites remaining un

167 mal (a condition achieved with an SR calcium channel opening drug) and partially when depletion was l

168 rials are needed to evaluate the value of BK channel opening drugs or gene therapies for NDO treatmen

169 , mouse muscle fibres did not respond unless channel-opening drugs were present at substantial concen

170 lcium channels, a low probability of calcium channel opening during an AP, and the rare triggering of

171 However, the mechanism of channel opening during translocation is unclear.

172 ings of unitary LTCC currents confirmed rare channel openings during depolarization of venous compare

173 ves" because they are initiated by L-type Ca channel openings during the action potential.

174 Compared to the unusually brief single-channel opening episodes elicited by agonist alone, chan

175 opening episodes elicited by agonist alone, channel opening episodes in the presence of agonist and

176 This results in an increase in the channel-opening equilibrium constant ((Phi(-1) = k(op)/k

177 en accounted for by a 5-fold decrease in the channel-opening equilibrium of the mutated receptor comp

178 rgo sequential gating transitions leading to channel opening even before all VSDs have moved.

179 increasing the probability of L-Type Ca(2+) channel opening events.

180 Consistent with a postsynaptic channel opening, excitations were accompanied by a decre

181 We found that the channel opening extends from the pre-TM2 region through

182 o-fold with an EC(50) of 3 muM by increasing channel opening frequency without altering mean open tim

183 muscle AChRs from the open state and impairs channel opening from the resting state, (d) inhibits bin

184 loop 3 (CL3), which promotes ATP-independent channel opening, greatly weakened inhibition by Fe(3+) n

185 Although the essential steps leading to channel opening have been described, fundamental questio

186 ong the complete reaction coordinate for ion channel opening have never been observed.

187 linkers in any manner dramatically curtailed channel opening, highlighting the requirement for rearra

188 n Ca(2+) evoked release by modulating Cav1.4 channel openings; however, RIM1/2 are not needed for the

189 Effluent from donor vessels elicited K(+) channel opening in an iberiotoxin- or PEG-CAT-sensitive

190 pantel, but not AAD-2224, was able to induce channel opening in an irreversible manner at similar con

191 ot its inactive enantiomer AAD-2224, induced channel opening in an irreversible manner.

192 ausing the same level of [ATP](i) and K(ATP) channel opening in both groups, suggesting a decrease du

193 anding how the binding of cAMP is coupled to channel opening in HCN and related channels.

194 ly contributes to coupling ligand binding to channel opening in human alpha7 nAChR.

195 te at the bundle crossing is responsible for channel opening in response to a voltage stimulus, where

196 ctivation of protein kinase C (PKC) promotes channel opening in some channels but not others, consist

197 ostatic interaction also promotes unliganded channel opening in the absence of ATP binding and NBD di

198 Moreover, W610X results in hClC-Kb channel opening in the absence of barttin and prevents f

199 These results indicate that channel opening in the AMPA receptors is controlled by b

200 intracellular vestibule less splayed during channel opening in the presence of ATP.

201 d-phase lipids to enter the platform-staging channel opening in the thinner mobile neighborhood.

202 ed states whilst increasing the frequency of channel opening; in contrast, all these changes were rev

203 and that disturbance of its sequence allows channel opening independent of any sensor domain.

204 aviour of CFTR is characterized by bursts of channel openings interrupted by brief, flickery closures

205 nt constitutive openness, we propose that BK channel opening involves structural rearrangement of the

206 to an ionotropic glutamate receptor leads to channel opening is a central issue in molecular neurobio

207 In other words, channel opening is a highly concerted, switch-like proce

208 The iris-like channel opening is accompanied by an alpha-to-pi-helical

209 eagues use this mutation to demonstrate that channel opening is determined by the flexibility of a re

210 Progressive PANX1 channel opening is directly linked to permeation of ions

211 grate and convert physiological signals into channel opening is essential to understanding how they r

212 ch the C-linker becomes less structured, and channel opening is not facilitated.

213 signals within a nascent polypeptide trigger channel opening is not understood.

214 Channel opening is primarily stimulated by transmembrane

215 ore-operated Ca(2+) release-activated Ca(2+) channel opening, is impaired in Atg7-deficient T cells.

216 iate the coupling between Ca(2+) binding and channel opening, is specifically required for the beta2

217 -THDOC does not affect the rate constant for channel opening (k(op)) of approximately 250 s(-1) but d

218 as Sec63 protein, which assists BiP in Sec61 channel opening) led to increased Ca(2+) leakage via Sec

219 As a result, channel opening may involve transmembrane rearrangements

220 The results strongly support the channel opening mechanism proposed on the basis of avail

221 The results are consistent with the channel opening mechanism proposed on the basis of close

222 ation of the Schiff base, are coupled to the channel-opening mechanism remains elusive.

223 issue damage or visceral distension, induces channel opening, membrane depolarization, and initiation

224 a suggest that higher PAM occupancy promotes channel opening more efficiently and overcomes short and

225 in binding, but other arguments suggest that channel opening must be potentiated by downstream change

226 CHD2 does not encode an ion channel, opening new avenues for research into human cor

227 ll-attached patches but had little effect on channel opening on inside-out patches.

228 We propose Orai channel opening on SG membranes as a potential mode of c

229 go a single concerted movement that leads to channel opening, or (ii) individual voltage-sensor movem

230 with the tetrameric C-linker and facilitates channel opening, or by a transition of apo-HCN to monome

231 isecond range between Ca(2+) application and channel opening (pre-onset delay) and exhibits slower ki

232 cal channel-closing rate constant and thus a channel-opening probability of 0.85 vs 0.96 for rGluK2.

233 n ion current activation, suggesting that BK channel opening proceeds in two steps.

234 e information on the trigger that begins the channel-opening process.

235 nt of agonist binding energy realized in the channel-opening process.

236 GPCR-induced TRPC3c channel opening rate (cell-attached patch) matched the m

237 t V188M markedly decreased the apparent AChR channel opening rate and gating efficiency.

238 rs at similar concentrations, decreasing the channel opening rate and shifting the GABA concentration

239 n by equilibrium binding and on the receptor channel opening rate by a laser-pulse photolysis techniq

240 on disrupts biosynthetic processing, reduces channel opening rate, and decreases protein lifetime.

241 d that the human GluK2 has a ~3-fold smaller channel-opening rate constant but an identical channel-c

242 destly decreased E(2) (mainly by slowing the channel-opening rate constant) and sometimes produced AC

243 ibition of this aptamer on the AMPA receptor channel-opening rate process in the microsecond-to-milli

244 y increased the probability of BK(Ca) single-channel openings recorded from cell-attached patches, an

245 r mechanism by which ligand binding leads to channel opening remains poorly understood, due in part t

246 How ATP binding triggers channel opening remains unclear.

247 to protein conformational changes leading to channel opening remains unknown.

248 olecules required to prevent agonist-induced channel opening remains unknown.

249 und that short-lived channel closures during channel openings represent subtle changes in the structu

250 xpressed with MtrC, suggesting that the MtrE channel opening requires MtrC binding and is energy-inde

251 In these cells TRPC3 channel opening requires stimulation of metabotropic glu

252 A single TRPV4 channel opening resulted in a stochastic localized Ca(2+

253 th outwardly rectifying K(+) channels, where channel opening results from a final concerted transitio

254 formation, in addition to four other partial channel openings, richly illustrates the structural basi

255 Many K+ channel proteins, after initial channel opening, show a time-dependent reduction in curr

256 timuli, indicating that the agonist promotes channel opening similar to that of volume-dependent acti

257 hannels, whereas the R243W mutation disrupts channel opening solely in the presence of KCNE1 by right

258 r organic cations, to trigger the subsequent channel-opening step.

259 sulting in activity-dependent enhancement of channel opening termed Ca(2+) -dependent facilitation (C

260 GluN1 has a stronger ability in maintaining channel opening than the counterpart in GluN2A.

261 acceptor and plays a more important role in channel opening than the primary acceptor.

262 evation of CaV1 activity is apparent in late channel openings that can last for seconds following a d

263 l properties and suggest that transitions to channel opening, the behavior of the open channel, and r

264 n the hyperpolarizing stimulus and the first channel opening, the first latency, determines the activ

265 t is also well known that accompanying KCNQ1 channel opening, the ionic current is suppressed by a ra

266 inding has been shown to promote CNG and HCN channel opening, the precise mechanism underlying gating

267 udies to understand better the regulation of channel openings, the dysfunction of CFTR in CF and the

268 mechanical energy into mechanosensitive ion channel opening, thereby generating electro-chemical sig

269 findings suggest that VX-770 can cause CFTR channel opening through a nonconventional ATP-independen

270 stream of, MARCKS is also required for TRPC1 channel opening through a similar gating mechanism invol

271 at p.V1184A shifts the voltage dependence of channel opening to hyperpolarized potentials thereby con

272 the binding of Ca(2+) ions before inhibiting channel opening to provide vital feedback inhibition.

273 , i.e., the ensemble average distance from a channel opening to the first obstruction.

274 explain the much lower efficacy of L-type Ca channel opening to trigger local SR Ca release at low [C

275 ted with a marked increase in the percent of channel openings to a subconductance level approximately

276 ons increasing the frequency and duration of channel openings to a submaximal state.

277 served VGCC-dependent minis, although single channel openings triggered release with low probability.

278 lve by releasing small osmolytes through the channel opening under extreme hypoosmotic conditions.

279 tive capture of cells in a single separation channel, opening up the possibility of multiple cell sor

280 s atropine-sensitive blockade of spontaneous channel opening upon coexpression of alpha6 and beta4 su

281 ur voltage sensor domains (VSDs) followed by channel opening via a last concerted cooperative transit

282 binations and in tandem dimers revealed that channel opening was slowed by Zn(2+) only when at least

283 .7 ms, n = 5 each) but that the amplitude of channel openings was reduced.

284 ling to the pore generates voltage-dependent channel opening, we solved the crystal structure and cha

285 emperature coefficient (Q10) of 18), and the channel openings were accompanied by large changes in en

286 mented because the frequency and duration of channel openings were increased.

287 Channel openings were inhibited by the ATP synthase inhi

288 process connecting glutamate binding to ion-channel opening, which is central to NMDAR physiology an

289 cket and the turret-like architecture during channel opening, which is consistent with a site of acti

290 disrupted heat sensitivity by ablating long channel openings, which are part of the temperature-gati

291 ctivation time course is mainly dependent on channel opening whilst slowly adapting current kinetics

292 In peptide-free CA3 cells, prolonging channel opening with a site-3 toxin, anemone toxin II, r

293 VSD movements are coupled to BK channel opening with a unique allosteric mechanism and a

294 Three sensors suffice to promote channel opening with FL(4)-like voltage dependence at de

295 to desensitize alpha4beta2 nAChRs and induce channel opening with higher affinity, but lower efficacy

296 olecular determinants of desensitization and channel opening with limited efficacy by the partial ago

297 of D97 to arginine (D97R) causes spontaneous channel opening, with open and closed dwell times simila

298 The first is voltage dependent and precedes channel opening, with properties consistent with reporti

299 m of CDI reduction is likely due to enhanced channel opening within the Ca(2+)-inactivated mode.

300 ion between the separating TM domains during channel opening would be facilitated in P2X2(I328C) rece