ライフサイエンスコーパス: channel pore

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

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

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

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

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

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

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

8 toplasmic domains that are propagated to the channel pore.

9 local anesthetic receptor within the sodium channel pore.

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

11 ubunit binding site in the I-II loop and the channel pore.

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

13 esting that TRPC1 subunits contribute to the channel pore.

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

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

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

17 ular vestibule and stabilization of the open channel pore.

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

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

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

21 ified two possible TETS binding sites in the channel pore.

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

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

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

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

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

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

28 conclusion that amantadine binds inside the channel pore.

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

30 subunits are essential components of the ARC channel pore.

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

32 n interactions between permeant ions and the channel pore.

33 p of GLUex results in an open, or near-open, channel pore.

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

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

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

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

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

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

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

41 could cause gross structural changes to the channel pore.

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

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

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

45 direct modulation of IS6 movement within the channel pore.

46 each subunit contributing to the functional channel pore.

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

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

49 ining regions of permanent charge within the channel pore.

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

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

52 nsitization and enhance ion flux through the channel pore.

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

54 ization, which are coupled to opening of the channel pore.

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

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

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

58 f its four N-termini enters and occludes the channel pore.

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

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

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

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

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

64 tage sensor movement and current through the channel pore.

65 ockade can concur simultaneously in the hERG channel pore.

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

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

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

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

70 inds to an extracellular vestibule above the channel pore.

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

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

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

74 novalent ions by directly blocking the TRPP2 channel pore.

75 barrier rather than steric occlusion of the channel pore.

76 he electric permittivity and diameter of the channel pore.

77 onformational changes into the gating of the channel pore.

78 dynamically favored down binding mode in the channel pore.

79 ditional state, GLUex rotates to occlude the channel pore.

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

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

82 of ion channel gating that engage the nAChR channel pore.

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

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

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

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

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

88 ir possible function as components of cation channel pores.

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

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

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

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

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 a Brownian particle moving through a gating channel pore and adjacent internal and external vestibul

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

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

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

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

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

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

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 Ligands bind to receptors, ions flow across channel pores, and transmitters and metabolites are tran

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

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

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

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

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

127 ge reduction also dramatically affected open channel pore block.

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

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

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

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

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

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

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

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

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

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

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

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

140 ates a new precedent whereby features of the channel pore can be modulated by exogenous drugs that bi

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

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

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

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

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

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

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

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

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

154 in the cavity located above the putative ion channel pore, for site-specific conjugation with a photo

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

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

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

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

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

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

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

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

163 s, of the intracellular S0-S1 loop of the BK channel pore-forming alpha-subunit controls functional c

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

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

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

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

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

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

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

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

172 en subpopulations of AC5 and the L-type Ca2+ channel pore-forming subunit CaV1.2.

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

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

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

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

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

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

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

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

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

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

183 ve long been thought to be determined by the channel pore-forming subunits.

184 rmacology of GABA(A)Rs are determined by the channel pore-forming subunits.

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

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

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

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

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

190 alysis of the interaction of PAX with the BK channel pore gate domain guided by recently available li

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

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

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

194 4.5 A, the structure for the membrane-bound channel (pore) has not been determined.

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

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

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

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

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

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

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

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

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

204 100 deg, exposing different residues to the channel pore in the open and closed states.

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

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

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

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

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

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

211 K115 into a tetra-tryptophan cage at the ion channel pore intracellular entrance.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

232 imately twofold symmetric arrangement of ion channel pore loops.

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

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

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

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

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

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

239 hy that changes a residue located in the ion channel pore of the GluN2A NMDA receptor subunit.

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

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

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

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

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

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

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

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

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

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

250 fected HEK 293 cells have phagocytic but not channel, pore, or membrane-blebbing function, and double

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

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

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

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

255 structural framework for understanding CRAC channel pore properties.

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

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

258 ics simulations revealed constriction of the channel pore radius to 2.4 angstrom as a result of the m

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

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

261 Ca(2+) that permeates through the channel pore regulates Ca(2+) affinities of coupled inhi

262 ure-dependent first step, sensitization, the channel pore remains closed while S6 helices undergo alp

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

264 nsitive relief of Ca(2+) inactivation of the channel pore selectivity filter.

265 ines local anesthetic binding effects to the channel pore, should be revised to include drug interact

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

267 CTX plugs the external mouth of K(+)-channels pore, stopping K(+)-ion conduction, without ind

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

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

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

271 coupled dilation of cytoplasmic LRRs and the channel pore, suggesting a mechanism for channel gating

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

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

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

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

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

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

278 jecture that Ca(2+) enters through the Na(V) channel pore, the optically resolved I(Ca) in the axon i

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

280 ermore, in all conformations displaying open channel pores, the N terminus of one subunit of the chan

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

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

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

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

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

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

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

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

289 o better match the respective surface of the channel pore vestibule.

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

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

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

293 trance of the nano-pockets and distal to the channel pore we generate an allosteric response in the a

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

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