ライフサイエンスコーパス: channel opening

1 tion that was blocked by inhibition of TRPV4 channel opening.

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

3 ng rearrangements that are necessary for ion channel opening.

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

5 lix to the plasma membrane potentiates CNGA1 channel opening.

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

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

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

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

10 al for coupling cyclic nucleotide binding to channel opening.

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

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

13 stsynaptic processes occurring after GABAA-R channel opening.

14 the synapse and by directly gating receptor channel opening.

15 itions substantially inhibited ATP-dependent channel opening.

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

17 olecular coupling between ligand binding and channel opening.

18 te, but modify coupling of ligand binding to channel opening.

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

20 oltage and temperature sensor activation and channel opening.

21 bsequently binds to TRPC1 subunits to induce channel opening.

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

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

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

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

26 ed SOCs, through regulating PIP(2) -mediated channel opening.

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

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

29 oltage dependent and closely correlates with channel opening.

30 lular ligand is coupled to the transmembrane channel opening.

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

32 native portion of the substrate against the channel opening.

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

34 modulation of ligand binding and subsequent channel opening.

35 ral movement of this domain results in anion channel opening.

36 ct both the second conformational change and channel opening.

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

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

39 ntry within the dendritic spine that follows channel opening.

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

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

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

43 e negatively charged residues, thus favoring channel opening.

44 hed conformational changes necessary for ion channel opening.

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

46 agonist binding, receptor preactivation, and channel opening.

47 ements following ligand binding resulting in channel opening.

48 closing at substantially lower tensions than channel opening.

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

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

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

52 ng GluN1 gating movements immediately before channel opening.

53 cessary and sufficient for TRIP8b to inhibit channel opening.

54 onal changes that then trigger regulation of channel opening.

55 multiple voltage sensors before KCNQ1/KCNE1 channel opening.

56 defects and potentiation to further increase channel opening.

57 lian Ca(2+)- and voltage-activated K(+) (BK) channel opening.

58 ions, thereby increasing the probability of channel opening.

59 t destabilizes these interactions to promote channel opening.

60 which the membrane deformation changes upon channel opening.

61 or cytosolic constriction conduct ions upon channel opening.

62 which TRPV1 translates diverse stimuli into channel opening.

63 side the intracellular vestibule, precluding channel opening.

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

65 gating charge movement, and its coupling to channel opening.

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

67 and synchronizes initial ligand binding with channel opening.

68 s major structural rearrangements leading to channel opening.

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

70 1(F246S) mutations also produced spontaneous channel openings.

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

72 K also diminished noticeably the duration of channel openings.

73 , it significantly enhanced the frequency of 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 ease of the Glu167/Arg290 salt bridge during channel opening allows a strong ionic interaction betwee

77 Channel opening allows signal sequence insertion into a

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

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

80 We conclude that the IT mutation stabilizes channel opening and alters ion selectivity of Ca(v)1.4 i

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 Ion channel opening and closing are fundamental to cellular

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

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

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

87 cit formulas in terms of SR [Ca] and release channel opening and closing rates.

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 Whether TARPs affect the rate of AMPA channel opening and closing, however, remains elusive.

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

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

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

96 e lateral plane contributed cooperatively 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 in animal Shaker-like channels that lead to channel opening and closing.

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

101 tating HG residues independently accelerated channel opening and compromised the closed state.

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

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

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

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

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

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

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

109 prolonging GABA(B) receptor activity promote channel opening and intensify oscillations.

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

111 g tool to study conformational changes after channel opening and may significantly advance the analys

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

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

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

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

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

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

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

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

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

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

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

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

124 However, how covalent modification leads to channel opening and, importantly, how noncovalent bindin

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

126 inct active state characterized by prolonged channel openings and low Ca(2+) permeability.

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

128 1a TARP) and gamma-4 (a type 1b TARP) on the channel-opening and channel-closing rate constants (i.e.

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

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

131 Cn2 facilitates Na(V) 1.6 early channel opening, and increased persistent and resurgent

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

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

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

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

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

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

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

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

140 channel functional properties, accelerating channel opening at more hyperpolarized membrane potentia

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

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

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

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

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

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

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

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

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

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

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

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

153 ion of TRPV3 by RTx requires facilitation of channel opening by introducing mutations in the pore, te

154 the pore, forming a physical gate, and that channel opening by iris-like motions simultaneously relo

155 d to phosphorylate TRPC1 proteins to promote channel opening by phosphatidylinositol 4,5-bisphosphate

156 ndent phosphorylation of TRPC1 essential for channel opening by phosphatidylinositol 4,5-bisphosphate

157 operated PKCdelta activity is obligatory for channel opening by PIP(2) , the probable activating liga

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

159 nucleotide-binding domain (CNBD) facilitates channel opening by relieving a tonic inhibition exerted

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

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

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

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

164 ling pathway in which a Piezo1-induced TRPV4 channel opening causes pancreatitis.

165 nd the selectivity filter gate, that control channel opening, closing, and inactivation.

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

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

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

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

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

171 rotation acts as a gating switch that tunes channel opening depending on the conformation of the mem

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

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

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

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

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

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

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

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

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

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

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

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

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

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

186 alpha7 with its homologs that cannot trigger channel opening has not been made so far.

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

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

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

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

191 they displayed noninactivating currents upon channel opening; i.e., hKv2.1-T377A and hKv3.1-T400A rem

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

208 thelial cells and that Piezo1-mediated TRPV4 channel opening is a function of the strength and durati

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

210 The iris-like channel opening is accompanied by an alpha-to-pai helica

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

212 Channel opening is also associated with changes in occup

213 we find that irrespective of stimuli, TRPP2 channel opening is dependent on activation of its VSDs.

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

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

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

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

218 Channel opening is primarily stimulated by transmembrane

219 Lateral channel opening is triggered by Sec63 interacting both w

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

221 anism of action resembles that of endogenous channel-opening lipids and opens up an avenue for the de

222 ant in a pre-open conformation suggests that channel opening may occur through a rotation of the intr

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

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

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

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

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

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

229 ylated derivatives of Br-PBTC can potentiate channel opening of alpha5-containing nAChRs.

230 Unlike other channels, opening of the pore is due to the repositionin

231 ll excitability through inhibition of K(ATP) channels, opening of voltage-dependent calcium channels,

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

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

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

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

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

237 s more slowly, without appreciable change of channel opening probability.

238 respectively, without appreciable change of channel-opening probability, as compared with GluA4 chan

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

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

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

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

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

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

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

246 es the CFTR maturation process and slows the channel opening rate.

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

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

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

250 How ATP binding triggers channel opening remains unclear.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

265 Upon channel opening, the curved transmembrane domain of MSL1

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

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

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

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

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

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

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

273 he weakly temperature-dependent second step, channel opening, tight association of the S1-S4 and pore

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

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

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

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

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

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

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

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

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

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

284 Tmc1 p.D569N, the resting probability of MET channel opening was smaller.

285 .7 ms, n = 5 each) but that the amplitude of channel openings was reduced.

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

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

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

289 Channel openings were inhibited by the ATP synthase inhi

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

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

292 ptor potential vanilloid subfamily 4 (TRPV4) channel opening, which was responsible for the sustained

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

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

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

299 stabilizes the channel structure and impairs channel opening without altering cilia localization and

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