ライフサイエンスコーパス: open channel

1 o relax away from the pore axis to create an open channel.

2 ared to conventional microfluidic SERS in an open channel.

3 each binding step in both the closed and the open channel.

4 cleavage site) resulted in a constitutively open channel.

5 are exposed in the permeation pathway of the open channel.

6 due to a decreased rate of flux through the open channel.

7 1a- 3) both activate the AChR and block the open channel.

8 and R237 residues produced a constitutively open channel.

9 ith KCNE3 (Mirp2) producing a constitutively open channel.

10 as a deformed beta-like conformation in the open channel.

11 channels is related to a fast flicker of the open channel.

12 a monomeric eight-stranded barrel lacking an open channel.

13 the conformational transition from closed to open channel.

14 ecting the countercharge centers favored the open channel.

15 ered channel gating and current flow through open channels.

16 the full-length beta4 protein did not block open channels.

17 oes not result from memantine escape through open channels.

18 ng the low flow resistance commensurate with open channels.

19 nly about 5% of the OprF population produced open channels.

20 teine was greater in closed channels than in open channels.

21 in response to Ca(2+) microdomains near the open channels.

22 in-of-function effect leading to permanently open channels.

23 clude the orientation, length, and number of open channels.

24 These open channels allow the diffusion of oxygen molecules wi

25 s 24 Si atoms per unit cell (oC24), contains open channels along the crystallographic a-axis that are

26 Next, both a single open channel and an array of parallel channels were test

27 al rates of cation translocation through the open channel and this is achieved at the expense of the

28 s(-1) and 22 s(-1), respectively, for Nav1.4 open channels and 7.1 microM(-1) s(-1) and 14 s(-1), res

29 for the current-voltage relationships of an "open" channel and they also show several subconducting t

30 conductance-voltage relation, decreases mean open-channel and burst duration by about sixfold, and re

31 consumption by >75%, but in Drosophila light opens channels and increases consumption 5-fold.

32 NP(o) x i(Ca) (where NP(o) is the number of open channels), and NP(o) and i(Ca) both depend on V(m).

33 ions to channel opening, the behavior of the open channel, and recovery from the desensitized state c

34 the GluN2A M3 helices from the lumen of the open channel, and reveals why the Lurcher mutation in Gl

35 the observation that phencyclidine (PCP), an open channel antagonist of the NMDA subtype of glutamate

36 Additionally, we provide evidence that open channels are required for glycine receptor inhibiti

37 domain composition in a manner that favours open channel area expansion, as well as allowing diffusi

38 ntified cytosolic Ca(2+)-binding site in the open channel as the Ca(2+) ions pass through the pore.

39 Fe(2)(+) of approximately 20 ions/s for each open channel at -60 mV and pH 7.2, with 1 muM extracellu

40 We developed a model of the activated, open channel based on the structure of the open MthK cha

41 t increase resulted from DC6C binding to the open-channel based on its prevention by proadifen, a non

42 n alpha-helix, and we propose a model of the open channel, based on MthK, in which Phe-1579 and Val-1

43 As confirmed by docking calculations, the open channel binds amantadine at the more favorable inte

44 gative voltages, permitting recovery from an open channel block along with a flow of current.

45 preparation to test the recent proposal that open channel block of the acetylcholine receptor by acet

46 ctivation, but Mg caused a greater degree of open channel block than Ca, making it unlikely that Kir1

47 the channel at negative membrane potentials (open channel block) by the nucleotide and not by a phosp

48 ly that of QX-314 was consistent with simple open channel block.

49 nhibition was noncompetitive, but not due to open channel block.

50 e use-dependent inhibition characteristic of open channel block.

51 cs for these agents are inconsistent with an open channel block.

52 bilization of closed states and low-affinity open channel block.

53 nt models via a dual allosteric mechanism of open-channel block and NO/redox modulation of the recept

54 show that diminazene blocks ASIC1a by a slow open-channel block and suggest that diminazene is an int

55 g cells of the cerebellum, are subject to an open-channel block and unblock by an endogenous protein.

56 v1.5 mutant to show that fluoxetine displays open-channel block behavior.

57 tage-dependent blocking kinetics indicate an open-channel block mechanism, which can be well describe

58 nt currents arise after relief of ultra-fast open-channel block mediated by an endogenous blocking pa

59 g that, like in NaV1.6-expressing cells, the open-channel block of NaV1.1 and NaV1.2 subunits is regu

60 ting that these residues are required for an open-channel block that approximates physiological resur

61 olarization, which results from relief of an open-channel block that terminates current flow at posit

62 were prolonged and the voltage dependence of open-channel block was reduced relative to control cells

63 aV1.6 is not unique in its susceptibility to open-channel block, because under appropriate conditions

64 re fast inactivation, slow inactivation, and open-channel block, we recorded voltage-clamped, tetrodo

65 tion of the few highly conserved residues to open-channel block, we synthesized several mutant peptid

66 late the susceptibility of alpha subunits to open-channel block, we voltage clamped wild-type and med

67 y 3alphaCOOH5betaP is consistent with simple open-channel block, with voltage dependence reflecting i

68 (the beta4 peptide), which mimics endogenous open-channel block.

69 importance of different residues in inducing open-channel block.

70 surgent current by controlling the extent of open-channel block.

71 of the experiment, and resembled a standard open-channel block.

72 s, which suggests that SI may interfere with open-channel block.

73 is favored by inactivation but prevented by open-channel block.

74 g the rate of block of NMDA receptors by the open channel blocker MK-801, we confirmed that the initi

75 anced charge transfer in the presence of the open channel blocker MK-801.

76 sis approaches, we identified citrate as an "open channel blocker" of AtALMT9 and used this tool to e

77 out a prepulse was completely blocked by the open channel blocker, (+)-5-methyl-10,11-dihydro-5H-dibe

78 using MK-801, an N-methyl-D-aspartate (NMDA) open channel blocker, implicates glutamate receptors in

79 a partial agonist, but can be blocked by an open channel blocker, picrotoxin.

80 by MK801 (dizocilpine hydrogen maleate), an open channel blocker, this potentiation was attributable

81 potential and/or Memantine, an NMDA receptor open channel blocker, would reduce noise-induced loss of

82 involve the voltage-dependent release of an open channel blocker.

83 -dependent phosphorylation, inhibited by the open-channel blocker glibenclamide.

84 Moving the positive charge also restored open-channel blocker interactions that are lost in K95Q.

85 Argiope lobata, is a potent but nonselective open-channel blocker of ionotropic glutamate (iGlu) rece

86 We conclude that PhTX-343 mainly acts as an open-channel blocker of nAChRs with strong subtype selec

87 ogenous neurotransmitter L-glutamate and the open-channel blocker picrotoxin.

88 Thus, beta4 may be the endogenous open-channel blocker responsible for resurgent kinetics.

89 Treatment with quinidine, an open-channel blocker used to treat the human disorder, r

90 interpreted as deoxycholic acid acting as an open-channel blocker, which may relate to deoxycholic ac

91 tail of the beta4 subunit acts as a classic open-channel blocker.

92 Using open channel blockers as tool compounds and a combinatio

93 these data suggest that amiloride and other open channel blockers bind to sites revealed during the

94 he activation gate in the VSD is unknown and open channel blockers for VSDs have not yet been identif

95 Other NMDA open channel blockers ketamine and memantine showed a si

96 ribe a class of small molecules which act as open channel blockers on the Hv1 VSD and find that a hig

97 channels are dilating, and as a consequence open channel blockers such as amiloride are allowed deep

98 are clinically useful NMDA receptor (NMDAR) open channel blockers that inhibit NMDARs with similar p

99 petitive NMDA antagonists, more specifically open channel blockers, which may be alternatives to high

100 onate (TBPS) are GABA(A) receptor (GABA(A)R) open channel blockers.

101 les are known to inhibit the PD by acting as open channel blockers.

102 several D1 ligands act as voltage-dependent, open-channel blockers for NMDA receptors, regardless of

103 nto the future design of kinetically tunable open-channel blockers for the AChR.

104 ine toxins from spiders and wasps are potent open-channel blockers of ionotropic glutamate (iGlu) rec

105 CMS include cholinergic agonists, long-lived open-channel blockers of the acetylcholine receptor ion

106 ibition; this effect was largely occluded by open-channel blockers, suggesting that lidocaine binding

107 ean burst duration, indicating that a linear open-channel blocking mechanism is not applicable.

108 The results also demonstrate that a known open-channel blocking peptide not only permits a rapid r

109 Thus, the open-channel blocking protein responsible for resurgent

110 current express an intracellular endogenous open-channel blocking protein, whose rapid binding upon

111 ellar Purkinje neurons express an endogenous open-channel blocking protein.

112 rsion of KCNQ1 by hKCNE3 to a constitutively open channel, but prevented its inhibition of Kv4.2 and

113 transmembrane domain allowed blockade of the open channel by the MTS reagents MTSEA, MTSET, and MTSES

114 americ p7 complex, which forms a transiently-open channel capable of conducting ions in simulation.

115 R-enantiomer binds to the enhancing site on open channels, causing them to stay open longer.

116 oated with chitosan for DNA extraction in an open channel configuration without the need for an addit

117 roosmotic pumping principles, has a multiple open-channel configuration consisting of hundreds of par

118 This transition confers an open-channel configuration enabling passage of the DNA s

119 rocess of AMPA receptors is to stabilize the open channel conformation, presumably by its pivotal str

120 at nucleotide binding at ABP1 stabilizes the open channel conformation.

121 nel-closing rate constant by stabilizing the open channel conformation.

122 del of the nAChR agonist binding site in the open channel conformation.

123 tive inhibitor that selectively inhibits the open-channel conformation of AMPA receptors with nanomol

124 -channel conformation and the fully liganded open-channel conformation of different members of the ni

125 Here we report the crystal structure of an open-channel conformation of NavMs, the bacterial channe

126 ences in ligand binding, specifically to the open-channel conformation of the protein.

127 y site with equal or higher affinity for the open-channel conformation than for the closed-channel co

128 ion of the TM23 linker, and destabilized the open-channel conformation that can lead to inhibition of

129 ning transmembrane alpha-helices (M2) in the open-channel conformation, in terms of the excess free e

130 pofol molecules bound symmetrically shows an open-channel conformation.

131 ins and act by stabilizing the agonist-bound open-channel conformation.

132 ulates the transition between the closed and open channel conformations.

133 assembles and isomerizes between closed- and open-channel conformations we measured changes in the di

134 ion rate constants from both the closed- and open-channel conformations, have been estimated experime

135 agonists results in different alpha7 nAChRs open-channel conformations.

136 ion channels that "gate" between closed- and open-channel conformations.

137 Because the open channel conformer is likely to fold as a single dom

138 Gel filtration showed that the open channel conformers tended to occur in oligomeric as

139 ur model by mutations around the closed- and open-channel constriction sites (Gln-4933 and Ile-4937).

140 ctance and alter the direction and amount of open channel current rectification.

141 in the channel sufficient to account for the open channel current.

142 xide or NADP(+), induces a large increase in open channel current.

143 he C<-->O isomerization process; and 3), the open-channel current amplitude (i(0)), which reports whe

144 Open-channel current amplitude distributions were indist

145 ic receptors in which activation to form the open channel depends on the binding of possibly multiple

146 al single-channel current amplitude and mean open-channel duration but that homoquinolinate slows act

147 c) in which the helix is undistorted, and in open channels (e.g. MthK) in which the M2 helix is kinke

148 Both operations are programmed by carving open channels either longitudinally or perpendicularly t

149 istance to protein adsorption was studied by open-channel electrophoresis for bovine serum albumin la

150 the window current (250%) and increased late open channel events (250%).

151 rs bind with equal or higher affinity to the open-channel form and alleviate picrotoxin inhibition.

152 ity for the closed-channel form than for the open-channel form and thereby inhibits the receptor by d

153 finity to the picrotoxin-binding site on the open-channel form of the receptor and the closed-channel

154 s mechanism describes the time course of the open-channel form of the receptor as a function of gluta

155 dissociation constant of picrotoxin for the open-channel form of the receptor was approximately 5 ti

156 the formation of the dimer interface in the open-channel form of the receptor.

157 ne (ACh) receptor converts transiently to an open-channel form when activated by ACh released into th

158 ity for the closed-channel form than for the open-channel form, thus shifting the equilibrium toward

159 -induced equilibrium between the closed- and open-channel forms of the receptor.

160 x that markedly exceeds that expected if all open channels had simply closed.

161 the fluorescent molecule calcein through the open channel have been studied.

162 ing in the external end of the pore, whereas open channels have a narrowing midway, the length of TM2

163 Alternatively, conductance through open channels I(h) channels of the resting membrane may

164 re nonlinear in a way similar to macroscopic open-channel I/Vs, so divalent gamma was underestimated

165 Crystal structures of the open channel in combination with a wealth of biophysical

166 ated by current flowing through continuously open channels in HC membranes.

167 red AQP5 proteins retain the ability to form open channels in the cell membrane and conduct water.

168 e change produced by current flowing through open channels in the HC membrane should occur with no de

169 to BPV-MOF-Ir due to the presence of larger open channels in the mixed-linker MOFs.

170 anemone toxin anthopleurin B, which impairs open-channel inactivation, exclusively enhanced inward g

171 he resting configuration selectively impairs open-channel inactivation.

172 The average number of open channels increases by approximately 50% upon additi

173 Azietomidate acted primarily as an open channel inhibitor characterized by a bimolecular as

174 attenuated if applied in the presence of an open-channel inhibitor and showed voltage-dependent reco

175 ng by rapidly binding to allosteric sites on open channels, initiating a rate-limiting conformation c

176 Single-channel conductance of the fully open channel is approximately 85 pS, and it is permeable

177 is more stable at negative potential and the open channel is more stable at positive potential.

178 f the lipids, whereas the conductance of the open channel is much less sensitive to this parameter.

179 ws for rapid diffusion of oxygen through the open channels, leading to efficient and reversible quenc

180 th a unique single channel conductance, mean open channel lifetime, and sensitivity to the allosteric

181 channel sensitivity to vanilloids, a maximal open-channel lifetime could be achieved.

182 eurotransmitter-gated ion channels where the open-channel lifetime increases with the number of bindi

183 ptors with only one intact binding site, the open-channel lifetime is indistinguishable from receptor

184 its identical binding sites, we measured the open-channel lifetime of individual receptors in which f

185 t need to be occupied to achieve the maximal open-channel lifetime, thus revealing a unique interdepe

186 obile phase diminishes analyte dispersion in open-channel liquid chromatographic columns due to minim

187 Solute dispersion in open-channel liquid chromatography is often dominated by

188 in cation transport number and by pronounced open-channel low-frequency current noise with a peak at

189 on neglects the fact that Ca(2+) released by open channels may influence subsequent gating through th

190 V to +50 mV to rapidly increase and decrease open channel-mediated sarcoplasmic reticulum lumenal to

191 is proof of principle study, we developed an open-channel membrane device that allows long-term conti

192 Here we demonstrate the ability of the open-channel microfluidic platform to maintain the funct

193 We developed a simple open-channel microfluidic system that can circumvent the

194 are difficult to achieve using conventional open-channel microsystems made from glass or polymers.

195 Computational docking in the Kv1.2-based open channel model yielded a complex in which a pyrethro

196 er goal of the present study, an approximate open channel model, consistent with many experimental fi

197 Importantly, we find that our open-channel model is consistent with the RyR1 and cardi

198 ween propafenone and Phe656 are found in the open-channel model).

199 e of ion-pulling simulations produces a RyR1 open-channel model, which can provide insights into the

200 nces between the liganded closed-channel and open-channel models could be detected at the level of th

201 ons on an extensively validated model of the open-channel muscle AChR.

202 m was tested using curare to demonstrate the open channel nature of the block and by identifying meth

203 Memantine, an open channel NMDA-R antagonist prescribed as a memory-pr

204 evoked glutamate release, measured with the open-channel NMDA (N-methyl-D-aspartate) receptor antago

205 acts in a sequence-independent manner as an open-channel NMDAR antagonist at or near the Mg(2+) site

206 nce and selectivity stay virtually constant; open channel noise is at its minimum.

207 le channel openings of TRESK-2 showed marked open channel noise.

208 mIPSCs is accompanied by an increase in the open channel number and requires activity-dependent tran

209 CTZ inhibited the open channel of the GABA(C) receptor with a time constan

210 The results demonstrate that the open channel of the P2X7 receptor can allow passage of m

211 Here, we construct an open-channel on-chip electroosmotic pump capable of gene

212 nabling the end user to generate patterns of open-channels on demand by carving the porous material o

213 flux directly by binding in and blocking the open channel or indirectly by stabilizing closed states

214 maximization algorithm, taking the number of open channels (or molecules in the on-state) at each tim

215 hanges observed when open or both closed and open channel pairs are stabilized.

216 actions that stabilize closed channel pairs, open channel pairs, or both in a balanced fashion.

217 lizing neighboring closed-closed and/or open-open channel pairs.

218 ysis of the pH dependences of the gating and open channel parameters yielded similar pKa values close

219 he open probability of the water channel, or open-channel permeability.

220 ach subunit contributes symmetrically to the open channel permeation pathway.

221 rized in a mortar and pestle showed that the open channel persistence length was reduced from 50 to 6

222 stic for certain applications is the average open channel persistence length, i.e., the ensemble aver

223 charge reduction also dramatically affected open channel pore block.

224 nding characteristic of INX1 GJs but not the open channel pore function.

225 acellular vestibule and stabilization of the open channel pore.

226 likely candidate for the binding site of an open-channel pore blocker such as N-(2-naphthalenyl)-[(3

227 These motions result in a minimum open-channel pore radius of approximately 3 A formed by

228 e affinity change for ACh that increases the open channel probability (DeltaGB).

229 application of 1 mum Ins(1,4,5)P3 increased open channel probability (NP(o)) by approximately 3-fold

230 al [Ca] from 20 microM to 5 mM increased the open channel probability (Po) of native RyRs in SR vesic

231 crease was caused by an increase of both the open channel probability and the number of functional ch

232 hannel conductance (6 pS at pH 3) implies an open channel probability of 10(-6)-10(-4).

233 L-type Ca(2+) currents and the open channel probability of Cav1.3 channels were also re

234 In summary, our data show that the open channel probability of Cx57 GJs can be modulated by

235 gle-channel recordings showed an increase in open-channel probability due to a three- to fivefold inc

236 of these opposing actions determines the low open-channel probability, P(O), which controls the excit

237 Compared with focusing in an open channel, protein bands in the monolith-filled EFGF

238 ity for the closed-channel form than for the open-channel receptor form and inhibit the receptor; cla

239 osed channel, whereas menthol stabilizes the open channel, relative to the transition state.

240 al-organic framework (MOF) with two types of open channels, representing a MOF featuring a (4,8)-conn

241 To this end, we generated an open-channel RyR1 model using molecular simulations to p

242 istribution of current amplitudes within the open channel showed MS channels fluctuate between subcon

243 work illustrates the ability to increase MOF open channel sizes by using the mixed linker approach an

244 ially, quinidine intracellularly blocked the open channel so rapidly it overlapped with activation.

245 sition between the two open states (Val-86), open channel stability, and the hydrogen-bonding network

246 te in the dark and after illumination in the open channel state and (ii) time-resolved fluorescence q

247 We show that Rgc2 maintains Fps1 in the open channel state in the absence of osmotic stress by b

248 tate clearly shows that the formation of the open channel state is associated with a large conformati

249 as part of a cation selective filter in the open channel state of CaChR1 as well as other low-effici

250 is an authentic Ypk1 substrate and that the open channel state of Fps1 requires phosphorylation by Y

251 dium- and glutamate-independent constitutive open channel state that rarely transitions to complete t

252 uctures of GLIC hypothesized to represent an open channel state were published.

253 of the nAChR transmitter binding site in the open channel state with that of the ACh binding protein,

254 stabilizes the receptor in an agonist-bound open channel state, and the glycine/ivermectin complex a

255 sing rate, a measure of the stability of the open channel state, controls an apparent tendency of the

256 and maintain conformational symmetry in the open channel state.

257 ore potent inhibitor in that it inhibits the open-channel state approximately 5-fold stronger than BD

258 from the inserted intermediate state to the open-channel state in the insertion/translocation pathwa

259 the binding free energy of a ligand with the open-channel state is higher than that with the closed-c

260 y calculated for the ligand binding with the open-channel state is significantly lower than that for

261 y functional states (particularly the active open-channel state) were only resolved at moderate resol

262 d that both compounds preferably inhibit the open-channel state, although BDZ-2 is a more potent inhi

263 1.5 muM or by approximately 15-fold over the open-channel state.

264 te and agonists bind more favorably with the open-channel state.

265 hydrogen bonding interactions stabilize the open-channel state.

266 interacts with D993 in TM9 to stabilize the open-channel state; D993 is absolutely conserved between

267 human brain NMDA receptors in the activated "open channel" state would be useful for research on such

268 eir ability to rapidly switch from closed to open channel states in the presence of ligand.

269 e-limiting conformation change to stabilized open channel states.

270 lecular structures of MscL in the closed and open channel states.

271 ed ligand binding domain crystallizes in the open channel structure, the longer LRET distances would

272 ally considered an immutable property of the open channel structure, whereas gating involves transiti

273 del presented here differs from the liganded open-channel structure of GLIC in the pre-M1 linker, the

274 l from Caenorhabditis elegans (GluCl), whose open-channel structure was determined complexed with the

275 sistent with the RyR1 and cardiac RyR (RyR2) open-channel structures reported while this paper was in

276 contrast, alcohols inhibited constitutively open channels, such as IRK1 or GIRK2 engineered to stron

277 rs access the closed channel slower than the open channel, suggesting that the intracellular entryway

278 ups onto beta2E155C closed the spontaneously open channels, suggesting that beta2Glu155 is a control

279 tween the first transmembrane helices of two open channels, suggesting that the observed Arg-189 conf

280 ng by nearly 8-fold but is unable to inhibit open channels, suggesting that this toxin inhibits chann

281 These results, mapped onto a model of the open channel surrounded by five alpha-helical M2s, imply

282 We conclude that hAQP1 is a constitutively open channel that closes mediated by membrane-tension in

283 al blocker could bind to three states of the open channel that differed in the locations and number o

284 This open channel then serves as both a gateway and a templat

285 roaching 0.7 imply that, within the class of open channels, there is a subclass that is not permeable

286 ed PSA, called colominic acid, prolonged the open channel time of AMPA-R-mediated currents by several

287 that roscovitine preferentially binds to the open channel to slow deactivation.

288 from all inactivated states was slower, and open-channel unblock was less voltage-dependent than in

289 ses of memantine, a low to moderate affinity open channel uncompetitive N-Methyl-d-aspartate receptor

290 interact with a blocking protein that binds open channels upon depolarization and unbinds upon repol

291 for CE analysis in both coated and uncoated open channels was also demonstrated.

292 The binding of flecainide to open channels was further investigated in a non-inactiva

293 hat TBA can enter the cavity only through an open channel whereas Dauda can bind to the closed channe

294 eines from the cytoplasmic side is faster in open channels, whereas access to these same sites from t

295 channel closure and produces constitutively open channels, whereas the R243W mutation disrupts chann

296 binding to either of two inhibitory sites on open channels with bimolecular kinetics.

297 After filling the open channels with electrolyte solution, a meniscus form

298 rtz quadruple-barreled pipet and filling the open channels with electrolyte solution, and quasi-refer

299 xin that is able to convert the pump into an open channel, with consequent loss of cellular K(+) and

300 In cell-attached patches, number of open channels x open probability (NP(o)) of a 230-250 pS