ライフサイエンスコーパス: channel pore

1 tage sensor movement and current through the channel pore.

2 els of the open and closed state of the HCN2 channel pore.

3 BI-1-mediated Ca(2+) leak and its potential channel pore.

4 onducting lateral portals, and gating of the channel pore.

5 at the channel constriction site out of the channel pore.

6 perative drying and iris-like closing of the channel pore.

7 ate, all of which lead to the opening of the channel pore.

8 st binding site of the receptor or block the channel pore.

9 on of the amantadine-binding site inside the channel pore.

10 tional changes in CFTR structure to gate the channel pore.

11 s do not block small-molecule entry into the channel pore.

12 y in the peaks near the ends of the AChR ion channel pore.

13 conclusion that amantadine binds inside the channel pore.

14 sociated with the opening and closing of the channel pore.

15 subunits are essential components of the ARC channel pore.

16 l change from the short NR1 CT to the nearby channel pore.

17 n interactions between permeant ions and the channel pore.

18 , and a rather broad region 3 containing the channel pore.

19 sidues lie in the extracellular mouth of the channel pore.

20 ctivation and inactivation gates of the K(+) channel pore.

21 n the EM work and water molecules within the channel pore.

22 led when a single Ca(2+) ion is bound to the channel pore.

23 CM1 multimers form the Ca(2+)-selective CRAC-channel pore.

24 tribute to the ionic selectivity of the CRAC-channel pore.

25 represent that of a cyclic nucleotide-gated channel pore.

26 could cause gross structural changes to the channel pore.

27 r that may be associated with changes in the channel pore.

28 ht to be accompanied by rearrangement of the channel pore.

29 smembrane helix--the M2 helix--to create the channel pore.

30 direct modulation of IS6 movement within the channel pore.

31 each subunit contributing to the functional channel pore.

32 ciated with voltage-dependent binding in the channel pore.

33 steric barrier in the narrowest part of the channel pore.

34 ining regions of permanent charge within the channel pore.

35 at ultimately lead to the opening of the ion channel pore.

36 nus that contributes to the formation of the channel pore.

37 nsitization and enhance ion flux through the channel pore.

38 to simulate the docking of L-7 to the KCNQ1 channel pore.

39 so referred as pre-M2) that form part of the channel pore.

40 ility for this enantiomer of the drug in the channel pore.

41 hat inhibit Na(+) flux by blocking the Na(+) channel pore.

42 ctional and structural properties of the Na+ channel pore.

43 ost likely to involve a rearrangement of the channel pore.

44 at directly modulate the size of the central channel pore.

45 (Asp(315), Asp(349)) near the mouths of the channel pore.

46 av1.1, 1.2, and 1.6) that code for the Na(+) channel pore.

47 pha4 nicotinic receptor near the gate in the channel pore.

48 ins (cNBHD), which is directly linked to the channel pore.

49 olyze ATP; in CFTR this opens and closes the channel pore.

50 Ba(2+) block, suggesting an asymmetry of the channel pore.

51 Ala-30, Gly-34, His-37, and Trp-41 line the channel pore.

52 ally placed near the center of the cell-cell channel pore.

53 tward, suggesting multi-ion block within the channel pore.

54 ubunit and forms an integral part of the ion channel pore.

55 occupancy of a potassium binding site in the channel pore.

56 novalent ions by directly blocking the TRPP2 channel pore.

57 barrier rather than steric occlusion of the channel pore.

58 he electric permittivity and diameter of the channel pore.

59 onformational changes into the gating of the channel pore.

60 dynamically favored down binding mode in the channel pore.

61 ion of bile acids with a region close to the channel pore.

62 ockade can concur simultaneously in the hERG channel pore.

63 ble to drive voltage-dependent gating of the channel pore.

64 owing many ions per photon to flow through a channel pore.

65 Ca(2+) influx at approximately 9 nm from the channel pore.

66 locker QX-314 into these axons via the TRPV1 channel pore.

67 ng its receptor site at the vestibule of the channel pore.

68 es of these domains result in opening of the channel pore.

69 ctive passage of potassium ions via the K(+) channel pore.

70 esidues lie in the S6 segments that line the channel pore.

71 o reveal how glutamate binding opens the ion channel pore.

72 gonist-binding domain dimer interface or ion channel pore.

73 determine the open/closed transition of the channel pore.

74 ve subunits coassemble to form a central ion channel pore.

75 toplasmic domains that are propagated to the channel pore.

76 recovered and one mutant, ouf8, affected the channel pore.

77 local anesthetic receptor within the sodium channel pore.

78 NBD2 is translated into opening of the KATP channel pore.

79 ires dissociation of the C terminus from the channel pore.

80 esting that TRPC1 subunits contribute to the channel pore.

81 residue (K95) in the inner vestibule of the channel pore.

82 nt to the membrane, that funnels ions to the channel pore.

83 sly unseen ATP-binding motif and an open ion channel pore.

84 ular vestibule and stabilization of the open channel pore.

85 rtant for ultrahigh K+/Na+ selectivity of K+ channel pores.

86 e responsible for the formation of other ion channel pores.

87 ir possible function as components of cation channel pores.

88 charged/polar residues to face the solvated channel pores.

89 h, it is unclear that TMC1 is indeed the MET channel pore: 1) in other animals or tissues, mutations

90 Present work characterizes the MET channel pore, a region whose properties are thought to b

91 sent at the RyR2 C terminus, proximal to the channel pore, a sterically appropriate location that wou

92 es (3.4 e) positioned adjacent (15 A) to the channel pore adequately model the data (surface charge d

93 on of R91W mutant Orai1 subunits in the CRAC channel pore affects the overall magnitude of its conduc

94 because an N-terminal ball domain blocks the channel pore after activation-a process termed N-type in

95 because an N-terminal ball domain blocks the channel pore after activation.

96 ics of these ions while interacting with the channel pore allowed us to rationalize their permeation

97 e that produces architectural changes in the channel pore alpha-helical region.

98 aturally occurring point mutants in the A/M2 channel pore, among which the most common are S31N, V27A

99 f single polypeptides containing both an ion channel pore and a serine/threonine kinase (chanzyme).

100 re multifunctional, because they contain the channel pore and also anchor the protein in membranes.

101 , which stabilizes the open state of the ion channel pore and creates lateral, phospholipid-lined cyt

102 One site is located in the channel pore and equates with a noncompetitive inhibitor

103 gion to the transmembrane domains, where the channel pore and gate reside.

104 xtracellular vestibule of the receptor's ion channel pore and is accessible after receptor activation

105 Lys7 of kappa-PVIIA deeply inserted into the channel pore and other hydrogen bonds and by hydrophobic

106 llular association domain localized near the channel pore and required for channel function.

107 a position (residue 34) thought to face the channel pore and show that thiol modification of the Cys

108 receptors to carry calcium sensors near the channel pore and tested this as a reporter for P2X(2) re

109 itioned to form a Ca(2+) binding site in the channel pore and that E190 interacts less directly with

110 region of residues 4820-4841 adjacent to the channel pore and the 96 kDa segment containing the regio

111 its relation to water movement for the NavMs channel pore and to make realistic predictions of its co

112 issense mutations localized in the potassium channel pore and two missense mutations localized in the

113 on (reporting on crown partitioning into the channel pore) and the noise (reporting on crown dynamics

114 tween BL-1743, known to bind inside the A/M2 channel pore, and amantadine were exploited to demonstra

115 ting role for Val(27) at the entrance to the channel pore, and channel activation by viral exterior p

116 heir binding site both directly, through the channel pore, and indirectly, through the water cavity o

117 arged amine group predicted to penetrate the channel pore, antagonizing current flow, while the remai

118 terminants of Cl- ion permeation through the channel pore are not known.

119 gating and the architecture of the open ion channel pore are unknown.

120 ransjunctional electric field and within the channel pore, as in this position they could sense chang

121 ructure of the ligand-binding domain and the channel pore, as well as major structural rearrangements

122 ructure of the ligand binding domain and the channel pore, as well as major structural rearrangements

123 inct from the structural domains forming the channel pore, as well as previously characterized intera

124 s its inhibitory effect via occlusion of the channel pore associated with an open/inactivated conform

125 inity sites, has been suggested to block the channel pore based on its ability to induce partial cond

126 tion channels, we engineered a set of cation channel pores based on the nonselective NaK channel and

127 y dopamine D1 receptor ligands is due to the channel pore block rather than receptor-receptor interac

128 ge reduction also dramatically affected open channel pore block.

129 d by nonspecific surface charge screening or channel pore block.

130 ly candidate for the binding site of an open-channel pore blocker such as N-(2-naphthalenyl)-[(3,5-di

131 on of chelating agents EGTA or BAPTA, cation channel pore blockers, competitive inhibitors of Ca(2+)

132 Although K+ channel pore-blocking toxins show specific interactions

133 sn has little effect on the structure of the channel pore, but dramatically reduces drug binding to t

134 attributed to a central constriction in the channel pore, but experimental verification is lacking d

135 are hexamers of ORAI proteins that form the channel pore, but the contributions of individual ORAI h

136 ing domain (CNBD), which is connected to the channel pore by a C-linker region.

137 th large cytosolic structures, access to the channel pore by inactivation domains may occur through l

138 is caused by voltage-dependent block of the channel pore by intracellular Mg2+ and polyamines such a

139 nt occupancy of an anion-binding site in the channel pore by trans-anions.

140 s directly coupled to the opening of the ion channel pore by way of an iris-like expansion of the tra

141 ion-response curve into a range in which the channel pore can respond to dynamic changes in cytosolic

142 ar pore region, although binding outside the channel pore cannot yet be excluded.

143 lectron density (at 3.5 A resolution) in the channel pore, consistent with amantadine blocking the po

144 d applications of agonist, and the intrinsic channel pore dilates to allow the passage of fluorescent

145 raised concerning whether the prokaryotic K+ channel pore does actually represent those of eukaryotes

146 he key conformational changes of a potassium channel pore domain as it progresses along its gating cy

147 ated Kv1.1 channel alpha-subunit without the channel pore domain or the voltage sensor.

148 ion point mutations surrounding the putative channel pore domain were expressed and characterized in

149 eracting with a conserved Trp residue in the channel pore domain.

150 CN4-G482R is located in the highly conserved channel pore domain.

151 previously uncharacterized function for the channel-pore domain as a regulator of channel traffickin

152 ed by intracellular loops extending from the channel pore domains has been referred to as a transmiss

153 tion have focused on the agonist binding and channel pore domains, relatively little is known about t

154 lices toward and away from the center of the channel pore during gating.

155 In the modeled channel, pore-facing regions of TM1 and TM2 were highly

156 operty, we engineered a set of mimics of CNG channel pores for both structural and functional analysi

157 ent pre- and post-M2 regions are involved in channel pore formation, cation selectivity, and amilorid

158 ium (K(ATP)) channel and thereby closing the channel pore (formed by four Kir6.2 subunits).

159 can produce enhanced activity of the K(ATP) channel pore (formed by Kir6.2).

160 ealed the presence of a large number of K(+) channel pore forming (alpha) and accessory (beta) subuni

161 A large number of voltage-gated K+ channel pore-forming (alpha) and accessory (beta, minK,

162 nstrating a role for voltage-gated K(+) (Kv) channel pore-forming (alpha) subunits of the Kv4 subfami

163 st the hypothesis that voltage-gated K+ (Kv) channel pore-forming (alpha) subunits of the Kv4 subfami

164 The channel pore-forming alpha subunit Kv4.2 is a major cons

165 solic carboxyl terminus of the N-type Ca(2+) channel pore-forming alpha(1B) subunit with the modular

166 expression of the cardiac voltage-gated Na+ channel pore-forming alpha-subunit (Na(v)1.5-alpha), the

167 fs in the intracellular C terminus of the BK channel pore-forming alpha-subunit that are conserved fr

168 occurred in the protein expression of Ca(2+) channel pore-forming alpha1A (P/Q-type), alpha1B (N-type

169 We co-expressed the calcium channel pore-forming alpha1C subunit with different acce

170 e levels of protein expression of the Ca(2+) channel pore-forming alpha1D (L-type) and alpha1E subuni

171 drogen bond between Ser165 and Thr141 in the channel pore-forming P-region that helps stabilise the s

172 In the ATP-dependent K+ (KATP) channel pore-forming protein Kir6.2, mutation of three p

173 Loss-of-function mutations in the CRAC channel pore-forming protein ORAI1 or the Ca(2+) sensing

174 romal interaction molecule 1 (STIM1) and the channel pore-forming protein Orai1.

175 ity with a peptide corresponding to the hERG-channel pore-forming region.

176 ilarities in the structural elements of K(+) channel pore-forming regions and postulated equivalent r

177 Ca(V)2.2a) splice variant of the N-type Ca2+ channel pore-forming subunit is recruited to presynaptic

178 se they form a channel complex with the K(+) channel pore-forming subunit Kv4.3 in a subset of nocice

179 The K(+) channel pore-forming subunit Kv4.3 is expressed in a sub

180 We report the identification of a new K(+) channel pore-forming subunit of the ether-a-go-go (Eag)

181 nnel by regulation of the interaction of the channel pore-forming subunit with different cellular pro

182 The channel pore-forming subunit, alpha1, and a regulatory s

183 mini of the ATP-sensitive potassium (K(ATP)) channel pore-forming subunit, Kir6.2, both lie intracell

184 the cell surface expression of alpha1c, the channel pore-forming subunit.

185 KCNQ2 and KCNQ3 ion channel pore-forming subunits coassemble to form a heter

186 5 members in a gene family that encodes K(+)-channel pore-forming subunits in Paramecium tetraurelia.

187 acts directly with two distinct sites of HCN channel pore-forming subunits to control channel traffic

188 Expressions of the K+ channel pore-forming subunits were not affected by IR, w

189 DPPX associates with the channels' pore-forming subunits, facilitates their traff

190 ormation of a bacterial voltage-gated sodium channel pore from Magnetococcus sp. (NaVMs) has provided

191 l block resulting from the drug entering the channel pore from the cytoplasmic side.

192 channel conformation of NavMs, the bacterial channel pore from the marine bacterium Magnetococcus sp.

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

194 per NPC per second) and the diameter of the channel pore (>15 nm) were estimated from the SECM data

195 ers, important for coupling Ca(V)beta to the channel pore, guided mechanistic functional studies.

196 In contrast, graded blockade of the Ca(2+) channel pore has a remarkably mild effect, although some

197 lthough high-affinity "block" of the open Na channel pore has been proposed.

198 The atomic structure of a bacterial K+ channel pore has been solved by means of X-ray crystallo

199 nstrates that PEG partitioning into the OmpF channel pore has sharper dependence on polymer molecular

200 4.5 A, the structure for the membrane-bound channel (pore) has not been determined.

201 Different conformational changes in the channel pore have been described during channel opening

202 tatic interactions between permeant ions and channel pore helix dipoles have been proposed as a gener

203 ar loop connecting domains II and III of the channel pore (II-III loop).

204 biturate binding site within the central ion channel pore in a closed conformation.

205 terized the function of a voltage-gated K(+) channel pore in a lipid membrane.

206 by binding to one or more subunits and (2) a channel pore in each subunit.

207 al aspartate residues in the proposed Ca(2+)-channel pore in full-length BI-1, we found that Asp-213

208 ytoplasmic end of S6 but resides deep in the channel pore in or near the selectivity filter.

209 hin the polynucleotide must pass through the channel pore in sequential, single-file order because th

210 ned more proximal to the central axis of the channel pore in the A/C conformation and S2-M4 more prox

211 tate, exposing different residues to the ion channel pore in the open and closed states.

212 The structure and reactivity of ion channel pores in general suggest that they will be a bro

213 rotective antigen (PA63) component to form a channel (pore) in the membrane of an acidic intracellula

214 P gates a phosphatase activity rather than a channel pore, indicating that VSDs function independentl

215 at the base of the thumb and residues in the channel pore influence proton inhibition in a voltage-in

216 f adenosine triphosphate-sensitive potassium channel pore inhibition in awake, fluid-resuscitated sep

217 have the same triplet of amino acids in the channel pore ion selectivity filter, and this sequence i

218 periments show that the open-diameter of the channel pore is >25 A, but the exact size and whether th

219 roach to demonstrate that the functional ARC channel pore is a heteropentameric assembly of three Ora

220 cently demonstrated that the functional CRAC channel pore is composed of a tetrameric assembly of Ora

221 In contrast to the CRAC channels, where the channel pore is composed of only Orai1 subunits, both Or

222 because the transfer of the K+ ion into the channel pore is energetically favoured, a feature common

223 cently demonstrated that the functional CRAC channel pore is formed by a homotetrameric assembly of O

224 for the first time, that the functional CRAC channel pore is formed by a tetrameric assembly of Orai1

225 The ryanodine receptor (RyR) channel pore is formed by four S6 inner helices, with it

226 Opening of the NMDA receptor ion channel pore is initiated by agonist-induced conformatio

227 These data suggest that the channel pore is lined by several transmembrane segments,

228 mantadine/rimantadine binding outside of the channel pore is not the primary site associated with the

229 ular Mg(2+) homeostasis in mammals since its channel pore is permeable to Mg(2+) ions and can act as

230 ytoplasmic side of the voltage-dependent Na+ channel pore is putatively formed by the S6 segments of

231 The H(37)xxxW(41) motif located in the channel pore is responsible for its gating and proton se

232 us, direct physical interaction with the ion channel pore is the basis of KCNE1 regulation of K+ chan

233 These data suggest that the channel pore is widened and ion selectivity is altered b

234 Selective ion conduction across ion channel pores is central to cellular physiology.

235 believed to interact with residues near the channel pore), it has distinctive features such as the a

236 lular Mg(2+), which act on both sides of the channel pore loop.

237 imately twofold symmetric arrangement of ion channel pore loops.

238 ified 2 more novel missense mutations in the channel pore (M373I) and the S6 transmembrane domain (S3

239 he NMDA receptor subtype, opening of the ion channel pore, mediated by displacement of the M3 helices

240 he other is the non-selective NaK2CNG, a CNG channel pore mimic.

241 The ability to construct a Na(+) channel pore model consistent with most of the available

242 by three macrocycle conformations with their channel pores observed as cc/oc/oo.

243 do not find a chlorpromazine molecule in the channel pore of ELIC, but behind the beta8-beta9 loop in

244 ns, allowing us to dock a voltage-gated K(+) channel pore of known structure onto the gating ring wit

245 azine is a widely used tool to probe the ion channel pore of the nicotinic acetylcholine receptor, wh

246 amino acid (alanine302) in the chloride ion channel pore of the protein.

247 tivity during the crosstalk, whereas the ion channel pores of the P2X receptors were fully functional

248 gion located at the cytosolic surface of the channel pore, on whole-cell K(+) currents, were studied

249 ve solute translocation pathways through the channel pore: One pathway transports anions nonselective

250 subtle geometric changes with the tennimide channel (pore) open (o) and/or closed (c), as noted by t

251 te binding and not by glycine binding nor by channel pore opening.

252 In ligand-gated channels, pore opening is conferred through transduction

253 tes the conductance of the receptor when the channel pore opens.

254 ng that the AI domain is associated with the channel pore or gating mechanism.

255 erves as a representation of a transmembrane channel, pore, or a carbon nanotube.

256 polyaniline (PANI) nanostructures within its channel pores (PANI/SBA-15) is synthesized and character

257 n modification in which toxin binding to the channel pore precedes maleimide alkylation of a nucleoph

258 l of the open/inactivated state of the Na(+) channel pore predicts, based on extensive mutagenesis da

259 NJ8 gene encoding the vascular Kir6.1 K(ATP) channel pore predisposed to an early and profound surviv

260 structural framework for understanding CRAC channel pore properties.

261 cal serine residue on the II-III loop of the channel pore protein.

262 These motions result in a minimum open-channel pore radius of approximately 3 A formed by Gln-4

263 , we show that this mutation affects the MET channel pore, reducing its Ca(2+) permeability and its a

264 on close to the intracellular opening of the channel pore regulate channel activity.

265 hannels and whether STIM1 contributes to the channel pore remains unknown.

266 no acid residue in the external mouth of the channel pore segment that is known to be involved in the

267 hat the delta2 receptor has a functional ion channel pore similar to that of glutamate receptors.

268 hannel, but which proteins contribute to the channel pore still needs to be determined.

269 We have found that multiple segments of the channel pore structure bind to the accessory protein KCN

270 The Kir channel pore structure was modeled by homology with the

271 we introduced cysteine residues in the CRAC channel pore subunit, Orai1, and probed their accessibil

272 ot consistent with predictions from the K(+) channel pore, suggesting that DEG/ENaC Na(+) channels ha

273 ing/channel gating coupling junction and the channel pore (T288N), which are functionally coupled dur

274 e a neutral glutamine (Q) residue within the channel pore that can be converted by RNA editing to a p

275 erimentally determined structure of a sodium channel pore that has a completely open transmembrane pa

276 vo SCAM", identified several residues in the channel pore that were exposed to the aqueous environmen

277 beta exerts toxicity is the formation of ion channel pores that disrupt intracellular Ca(2+) homeosta

278 The model depicts the channel pore, the channel gate, and the residues respons

279 The narrowest part of the channel pore, the selectivity filter formed by backbone

280 stal structure of a bacterial homolog of CNG channel pores, the NaK channel, revealed a Ca(2+) bindin

281 believed to lodge in the outer mouth of the channel pore, thereby stoppering ion flux.

282 fibrosis transmembrane conductance regulator channel pore: TMs 6 and 11 are close enough together to

283 of one or two binding sites, opening of the channel pore to a low conductance state when two sites a

284 allowing the parahelix to protrude into the channel pore to form the loop-gate barrier.

285 he key conformational change that causes the channel pore to open and close.

286 ineation of the ATP-binding site and the ion channel pore, together with the conformational changes a

287 ssibility method was used to explore calcium channel pore topology.

288 cytoplasmic acceptor located at or near the channel pore using the ball-and-chain machinery (1-5).

289 e-binding domain (CNBD) that connects to the channel pore via a C-linker domain.

290 2)(+) binding via the interactions among the channel pore, VSD and CTD.

291 A CNG1 channel pore was probed using site-directed cysteine sub

292 membrane electric potential across the GluR channel pore, we recorded from alpha-amino-3-hydroxy-5-m

293 ilibrium and dynamics in the confines of ion channel pores, we study partitioning of poly(ethylene gl

294 KIR6.2 forms a channel pore whose spontaneous activity and ATP sensitiv

295 TRPM6, are the only known fusions of an ion channel pore with a kinase domain.

296 The A419P mutation results in expanded channel pore with altered permeability that limits modul

297 second approach estimated dimensions of the channel pore with simple amine compounds.

298 llowing for the secretion of ATP through the channel pore with subsequent activation of purinergic re

299 ther blocking molecules that interact in the channel pore with the gating machinery can differentiall

300 annel-forming sequence and to define whether channel pores with enhanced conductive properties could