ライフサイエンスコーパス: shaker

1 y expressing a dominant-negative mutation of Shaker).

2 f free energy changes in BK S6 distinct from Shaker.

3 ating the sleep-modulating potassium channel Shaker.

4 ) female mice following exposure to platform shaker.

5 elucidates the electric field profile within Shaker.

6 nctive difference between these channels and Shaker.

7 rgent K(+) channels, ether-a-go-go (eag) and Shaker.

8 typically to assess synaptic transmission in Shaker.

9 kely responsible for impaired hearing in the shaker-1 mice.

10 motor function of a dimeric construct of the shaker-1 mutant.

11 However, the effect of the shaker-1 mutation, a R502P amino acid substitution, on t

12 afness/blindness syndrome in humans, and the shaker-1 phenotype, characterized by deafness, head toss

13 duction in the hair cells of young postnatal shaker 2 mice (Myo15(sh2/sh2)).

14 s of the abnormally short stereocilia in the shaker 2 mice did not show the characteristic tip densit

15 In adult shaker 2 mice, a mutation that disables the motor functi

16 Here we show that in young postnatal shaker 2 mice, abnormally short stereocilia bundles of a

17 al-hearing littermates, myosin-XVa-deficient shaker 2 mice, and whirler mice that have similarly shor

18 yrosine at Kv2.1 position 380 (equivalent to Shaker 449) with a threonine or cysteine had a relativel

19 ur side chains at the position equivalent to Shaker 449.

20 these applications, a homology model of the Shaker A channel permeation path was constructed using t

21 d with Shaker, suggesting that SSS modulates Shaker activity via a direct interaction.

22 ers accumulated over many generations, other Shaker alleles also become short sleepers and fail to co

23 ce map between the full-length and truncated Shaker alpha-beta complexes, a conformational change was

24 Experiments on hSkMI Na(+) channels and both Shaker and EAG K(+) channels indicate which S4 residues

25 e kinetics of K(v)1-type potassium channels (Shaker and K(v)1.2/2.1 chimera) through site-directed mu

26 the origins and functional evolution of the Shaker and KCNQ families of voltage-gated K(+) channels

27 differ significantly from that reported for Shaker and Kv1.4 channels.

28 hannel's structure due to differences in the Shaker and KvAP sequences.

29 al control of nerve terminal excitability by Shaker and Shab channels to confer temporal patterns of

30 division in synaptic regulation between the Shaker and Shab channels.

31 of voltage-gated A-type currents carried by Shaker and Shab, and the upregulation of voltage-indepen

32 The crystal structures of Shaker and Shaw T1 domains reveal interesting difference

33 genes and pathways modulating sleep, such as Shaker and sleepless, and candidate brain regions known

34 fect is caused by a concomitant loss of both Shaker and slowpoke (slo) channel activity because of th

35 necessary for the homeostatic modulation of Shaker and slowpoke expression.

36 to, the enhanced expression and function of Shaker and slowpoke.

37 ical vial, driven continuously by an orbital shaker and subjected to a symmetric confining centrifuga

38 the novel probe Di-1-ANEPIA to cysteines in Shaker and tracking field-induced optical changes, in vi

39 e include functional orthologs of bilaterian Shakers and channels with an unusually high threshold fo

40 ires the K(+) channel subunits Hyperkinetic, Shaker, and ether-a-go-go.

41 ey show that the K(+) channel genes shal and shaker are reciprocally regulated in the central nervous

42 two A-type potassium channel genes, shal and shaker, are reciprocally, transcriptionally coupled to m

43 o expressed and purified both WT and Delta C Shaker, assembled with the rat KvBeta2-subunit.

44 An up-and-down-shaker-assisted dispersive liquid-liquid microextraction

45 Our study focuses on the Shaker B ball peptide that is representative for rapid N

46 C-type inactivation mechanism as defined for Shaker B channels.

47 Each specimen was placed in a shaker bath containing de-ionized distilled water at 80

48 rated that SLEEPLESS (SSS) protein modulates Shaker channel activity, possibly through a direct inter

49 ng the proline residue P475 in the S6 of the Shaker channel by a glycine or alanine causes a consider

50 and serve to further diversify Nematostella Shaker channel gating properties.

51 stimulation, Slo effectively compensates for Shaker channel inactivation, stabilizing AP repolarizati

52 of the GORK (Guard Cell Outward Rectifying) Shaker channel mediating a massive K(+) efflux in Arabid

53 any similarities to that of mammalian Kv and Shaker channel models.

54 in patch-clamped cells were recorded from a Shaker channel mutant (M356C) labeled in the S3-S4 linke

55 identifying the role of the C-linker in the Shaker channel properties, we performed subdomain swappi

56 hese bridges provide constraints on the open Shaker channel structure, and on the degree of movement

57 Interestingly, mutations could tune Shaker channel to be either heat-activated or heat-deact

58 erologously expressing the voltage-dependent Shaker channel, we show that PIP(2) exerts 1) a gain-of-

59 similar to some of our earlier models of the Shaker channel.

60 nsmembrane and extracellular portions of the Shaker channel.

61 /K/Q/S or Y279F mutation whose equivalent in Shaker channels (T449E/K/D/Q/S or W434F) caused a greatl

62 zation and have revised our understanding of Shaker channels at this model synapse.

63 Shaker channels control the basal level of release, indi

64 Shaker channels have provided a powerful tool to establi

65 plication has produced highly unique sets of Shaker channels in the major metazoan lineages.

66 Hui1 is also specific, inhibiting KcsA-Shaker channels in Xenopus oocytes with a Ki of 0.5 nM w

67 coordination motif is conserved in other non-Shaker channels making this the most distinctive differe

68 s the activation of heterologously expressed Shaker channels with no effect on deactivation or fast N

69 of cysteines, one each in S4 and the pore of Shaker channels, and identified two instances of spontan

70 Contrary to Shaker channels, our work indicates that KCNQ1 channels

71 ype inactivation of heterologously expressed Shaker channels, providing a potential mechanism for the

72 ction recognized in drosophila with mutant ("shaker") channels: reduced sensitivity to isoflurane-ind

73 This generic model predicts well the Shaker charge/voltage and conductance/voltage relations;

74 the transient A-type K(+) current carried by Shaker cognate L (Shal; also known as voltage-gated K(+)

75 imensional structure of the Agitoxin (AgTx2)-Shaker complex.

76 Loss of the Shaker conductance attenuated the voltage signal and ind

77 hibited altered Shaker localization, reduced Shaker current density and slower Shaker current kinetic

78 n, reduced Shaker current density and slower Shaker current kinetics.

79 s accounts for nearly 40% of the decrease in Shaker current magnitude in flies lacking SSS.

80 ogous cells, SSS accelerated the kinetics of Shaker currents and was co-immunoprecipitated with Shake

81 ounts for the slower time-to-peak of in situ Shaker currents seen in qvr/sss mutants.

82 Additional experiments in Shaker demonstrated that TEA bound well to C-type inacti

83 evealed that quiver, a mutation that impairs Shaker-dependent potassium current, is an allele of slee

84 ely enhancing electrical excitability with a Shaker dominant-negative (SDN) potassium channel subunit

85 extracellular calcium (1.5 mM), the role of Shaker during AP repolarization is limited.

86 shaking behavior of mutants defective in the Shaker-encoded potassium channel, and temperature-sensit

87 -subunits that coassemble with Hk, including Shaker, Ether-a-go-go, and Ether-a-go-go-related gene, a

88 ion of sss in sss mutants rescued defects in Shaker expression and activity cell-autonomously and sug

89 oltage range where the channels were closed, Shaker expression had little effect on electromotility r

90 The F290L mutation in Shaker (F233L in K(v)1.2/2.1) accelerates channel closur

91 voltage-dependent potassium channels of the Shaker family (Kv1.2), normally localizing in the adjace

92 mational conservation between closed EAG and Shaker family channels, despite large differences in vol

93 In bilaterians, the Shaker family consists of four functionally distinct gen

94 Comparison of Shaker family gene complements from diverse metazoan spe

95 show that despite the strong conservation of Shaker family in plants, substantial differences can exi

96 The roles of potassium channels from the Shaker family in stomatal movements have been investigat

97 Thus, the Shaker family is metazoan specific but is likely to have

98 The Shaker family K(+) channel protein, Kv1.3, is tyrosine p

99 uctures based on a closed-state model of the Shaker family K+ channel Kv1.2 match these constraints.

100 SH3-dependent binding of Src family PTKs to Shaker family Kvs mediates modulatory events that are in

101 plants are structurally classified into the Shaker family named after the shaker K+ channel in Droso

102 Kv1.2 is a member of the Shaker family of voltage-sensitive potassium channels an

103 The Shaker family potassium channel, Kv1.2, is a key determi

104 g the x-ray crystal structure of a mammalian Shaker family potassium ion (K+) channel.

105 The Shaker family voltage-dependent potassium channels (Kv1)

106 The beta subunit (Kvbeta) of the Shaker family voltage-dependent potassium channels (Kv1)

107 We have investigated the behavior of Shaker family voltage-gated potassium (Kv) channels subj

108 Kv1 (mammalian Shaker family) potassium channels and the neurexin Caspr

109 P(2) effect on other Kv such as those of the Shaker family.

110 Finally, we show that short-sleeping Shaker flies have a reduced lifespan.

111 point mutation in a conserved domain of the Shaker gene.

112 Six of the Nematostella Shaker genes express functional homotetrameric K(+) chan

113 We identified 11 Nematostella Shaker genes with a distinct "silent" or "regulatory" ph

114 oreactivity is observed at the synapse; 3) a Shaker-GFP fusion protein that localizes to all type I b

115 transplanting the pore domain of TRPV1 into Shaker gives rise to functional channels that can be act

116 n Shaker K+ channels may help to explain why Shaker has an approximately tenfold lower conductance th

117 Voltage-gated potassium channels such as Shaker help to control electrical signalling in neurons

118 s relatively poor, as compared with that for Shaker IA channels and their Kv1 homologues.

119 functions are executed by the single OsK5.2 Shaker in rice.

120 els, as well as models of the pore domain of Shaker in the open and closed state.

121 he prototypical inactivating K+ conductance, Shaker, in Drosophila photoreceptors by recording intrac

122 The IL mutant of Shaker, in which the voltage dependence of channel openi

123 A reduction in Shaker increases the frequency of action potential firin

124 In contrast to ChTx.Shaker interaction, elevating [K](o) (from 2 to 98 mm) d

125 to discuss the role of the C-linker in plant Shaker inward channel structure and function.

126 tory bulb, in which it suppresses a dominant Shaker ion channel (Kv1.3) via tyrosine phosphorylation

127 Shaker is a low-conductance K-channel in which Pro475-->

128 Shaker is glycosylated on two asparagines (N259 and N263

129 in neurotransmitter release, suggesting that Shaker is predominantly responsible for AP repolarizatio

130 Shaker-iVSD also displays pronounced 'relaxation'.

131 Ion conduction in Shaker-iVSD developed despite identical primary sequence

132 Shaker-iVSD showed significantly altered gating kinetics

133 ted after the fourth transmembrane helix S4 (Shaker-iVSD).

134 iments employing macroscopic currents in the Shaker K channel have suggested a cytoplasmic localizati

135 nine F(290) located in the S2 segment of the Shaker K channel is an aromatic residue thought to inter

136 using histidine scanning mutagenesis in the Shaker K channel, we identified mutants I241H (S1 segmen

137 our segments of the VSD in the voltage-gated Shaker K channel.

138 ductance pathway for solution cations in the Shaker K(+) channel at rest.

139 anemone, including three subfamilies of the Shaker K(+) channel gene family: Shaker (Kv1), Shaw (Kv3

140 We examined the role of the outward Shaker K(+) channel gene OsK5.2.

141 s with qualitatively similar features to the Shaker K(+) channel in the absence of the N-terminal ina

142 Remarkably, the voltage-gated Shaker K(+) channel remains voltage gated after a 43 res

143 We probed similar interactions in the Shaker K(+) channel where inactivation was impaired in t

144 However, uncoupling the Shaker K(+) channel's pore domain (PD) from the VSD prev

145 In the voltage-gated Shaker K(+) channel, the mutation of the first arginine

146 d-type and charge-neutralized mutants of the Shaker K(+) channel.

147 Shaker K(+) channels form the major K(+) conductance of

148 Here we show that in nonconducting W434F Shaker K(+) channels, a large portion of this charge-vol

149 In Shaker K(+) channels, inactivation is caused by the cyto

150 mined the effects of La(3+) on voltage-gated Shaker K(+) channels.

151 ing-charge transfer for wild-type and mutant Shaker K(+) channels.

152 sleep and effect multiple changes in in situ Shaker K(+) currents, including decreased magnitude, slo

153 We studied the membrane electromotility of Shaker K(+)-transfected HEK-293 cells in real time by us

154 We investigated domain interactions in the Shaker K(v) channel by systematically mutating the pore

155 The method is applied to the Shaker K(v)1.2 potassium channel in implicit solvent.

156 Kv channel, Kv1.2, which is a member of the Shaker K+ channel family.

157 ified into the Shaker family named after the shaker K+ channel in Drosophila.

158 Both the Shaker K+ channel SHK-1 and the Ca2+/Cl--gated K+ channe

159 affinity of ion binding sites we probed the Shaker K+ channel with the quaternary ammonium analogue,

160 ructural models of AgTx2 in complex with the Shaker K+ channel, additional structural analysis provid

161 lecules attached to several positions in the Shaker K+ channel.

162 the latter experiments were performed on the Shaker K+ channel.

163 modelling, we show that the inactivation of Shaker K+ channels amplifies voltage signals and enables

164 the movement of these segments in functional Shaker K+ channels by using luminescence resonance energ

165 A narrower opening of the bundle crossing in Shaker K+ channels may help to explain why Shaker has an

166 In Shaker K+ channels no such transient fluorescence is obs

167 An early component of the gating current in Shaker K+ channels with a time constant of approximately

168 ur results demonstrate the importance of the Shaker K+ conductance for neural coding precision and as

169 Here we show that loss of the Shaker K+ conductance produces a marked reduction in the

170 y a qvr/sss transgene that fully rescues the Shaker kinetic phenotypes but only partially rescues the

171 tes more strongly with the effects of SSS on Shaker kinetics than current magnitude.

172 this fundamental question, we expressed the Shaker Kv channel at high levels and then measured macro

173 cordings of gating and ionic currents of the Shaker Kv channel expressed in Xenopus oocytes that F184

174 Furthermore, the inactivated Shaker Kv channel is readily blocked by bTBuA.

175 In contrast, bTBuA blockade of a Shaker Kv channel that undergoes open-state P/C-type ina

176 omain in the absence of the pore domain, the Shaker Kv channel was truncated after the fourth transme

177 Unlike the Shaker Kv channel, KvAP possesses an inactivated state t

178 g currents from gating pore mutations in the Shaker Kv channel, we identified statistically highly si

179 re protein motion at specific regions of the Shaker Kv channel.

180 regions of TRPV1 were transplanted into the Shaker Kv channel.

181 ng is similar to the well-studied eukaryotic Shaker Kv channel: conformational changes occur within f

182 cceleration of the VS kinetics in Nav versus Shaker Kv channels is produced by the hydrophilicity of

183 In contrast, blocking mediated by a Shaker Kv inactivation peptide is consistent with direct

184 dominated by the products of only two genes, Shaker (Kv1) and Shal (Kv4), both expressing voltage-dep

185 lies of the Shaker K(+) channel gene family: Shaker (Kv1), Shaw (Kv3) and Shal (Kv4).

186 Xenopus oocytes with a Ki of 0.5 nM whereas Shaker, Kv1.2, and Kv1.3 channels are blocked over 200-f

187 otent but promiscuous, blocking KcsA-Shaker, Shaker, Kv1.2, and Kv1.3 channels with Ki of 1-4 nM.

188 The Long-Evans shaker (les) rat has a mutation in myelin basic protein

189 ted auditory brainstems using the Long-Evans Shaker (LES) rat, a spontaneous mutant where compact mye

190 In this study, we used the Long-Evans shaker (les) rat, which can live up to 9 months, to stud

191 of normal axons and those of the Long-Evans shaker (LES) rat, which lacks compact myelin.

192 well known conformational changes in animal Shaker-like channels that lead to channel opening and cl

193 In Shaker-like channels, the activation gate is formed at t

194 increasing membrane excitability by removing Shaker-like K(+) channels, which are encoded by the Kcna

195 kt1 (Arabidopsis K(+) transporter) and skor (shaker-like K(+) outward-rectifying channel).

196 ce between cold-activated TRPM8 channels and Shaker-like Kv1.1-1.2 channels underlying the excitabili

197 MGE cell grafts in epileptic mice lacking a Shaker-like potassium channel (a gene mutated in one for

198 Mice lacking Kv1.1 Shaker-like potassium channels encoded by the Kcna1 gene

199 pore channels (TPCs) contain two copies of a Shaker-like six-transmembrane (6-TM) domain in each subu

200 pore channels (TPCs) contain two copies of a Shaker-like six-transmembrane (6-TM) domain in each subu

201 evelopmental stages 44-46, by overexpressing Shaker-like Xenopus Kv1.1 potassium channels using elect

202 ) loss-of-function mutants exhibited altered Shaker localization, reduced Shaker current density and

203 ecifically, Islet is sufficient to repress a Shaker-mediated A-type K(+) current, most likely due to

204 nd selectively suppresses fast-inactivating, Shaker-mediated IA currents in muscles.

205 In both Kv2.1 and Shaker, modification of cysteines at position 380/449 by

206 his system enabled stoichiometric control of Shaker monomers and the encoding of multiple amino acids

207 re incorporated into the N- or C- termini of Shaker monomers or within sodium channels two-domain fra

208 Among K+ channel transcripts, Shaker mRNA levels were preferentially increased in cac

209 yokymia/episodic ataxia type 1 (EA1) and the Shaker mutant phenotype in Drosophila.

210 recording intracellularly from wild-type and Shaker mutant photoreceptors.

211 degeneration of cerebellar Purkinje cells in shaker mutant rats can be modified: ablation of the infe

212 It is established that Shaker mutations cause a dramatic increase in neurotrans

213 sensorineural deafness in humans (DFNB3) and shaker (Myo15sh2) mice.

214 oncentrations following exposure to platform shaker or CCK administration (10 mug/kg i.p.) were not d

215 Some, but not all, mammalian Shaker or Kv1 alpha subunits contain a dominant endoplas

216 stricted interference with the expression of Shaker or Sandman decreased or increased sleep, respecti

217 rent in cultured myocytes was carried by the Shaker ortholog SHK-1.

218 ism for this higher conductance, we measured Shaker-P475D single-channel current in a wide range of s

219 large-scale physics do, however, differ for "shakers" (particles that are active but not self-propell

220 e outer-vestibule turret (Kv2.1 position 356/Shaker position 425), which has been shown to interfere

221 dy the binding process of kappa-PVIIA to the Shaker potassium channel and the structure of the result

222 ng the first S4 arginine by histidine in the Shaker potassium channel creates a proton pore when the

223 n of Kv1 channel functions, mutations of the Shaker potassium channel gene in Drosophila and the KCNA

224 sylation on the traffic of the voltage-gated Shaker potassium channel through the secretory pathway o

225 al changes underlying voltage sensing in the Shaker potassium channel, and it is superior at a site t

226 d accord with experimental estimates for the Shaker potassium channel, indicating that the final mode

227 In the Shaker potassium channel, mutation of the first arginine

228 By measuring gating currents from the Shaker potassium channel, we demonstrate here that short

229 ative to the pore domain in the prototypical Shaker potassium channel.

230 ll the K(v)AP model describes the Drosophila Shaker potassium channel.

231 udied the structure of the C terminus of the Shaker potassium channel.

232 to fit a series of gating currents from the Shaker potassium channel.

233 s to evaluate the resting-state model of the Shaker potassium channel.

234 In this method, proteoliposomes containing Shaker potassium channels are synthesized in vitro and i

235 y transfer a fluorescent based technique, to Shaker potassium channels expressed in live Xenopus oocy

236 served Trp434-Asp447 indole hydrogen bond in Shaker potassium channels with a non-hydrogen bonding ho

237 d these two issues, using both the Kv2.1 and Shaker potassium channels.

238 ice that had a gene-targeted deletion of the Shaker potassium ion channel (Kv1.3) to elucidate how ac

239 structure of MthK, the inner-pore helices of Shaker probably maintain the KcsA-like bundle-crossing m

240 Consistent with this finding, Shaker protein levels were reduced in sleepless mutants.

241 In Long-Evans shaker rats, loss of the Nav beta4 subunit specifically

242 st in the dysmyelinated axon from Long-Evans shaker rats, which lack compact myelin.

243 pecies encoding mouse Kv1.4, a member of the Shaker-related subfamily of voltage-gated potassium chan

244 Expression of voltage-gated K channel, shaker-related subfamily, member 5 (KCNA5) underlies the

245 Kv1.4 channels are Shaker-related voltage-gated potassium channels with two

246 re, we directly demonstrate that Kv1-family (Shaker-related) delayed rectifier K(+) channels in the c

247 e organic cation guanidinium, reminiscent of Shaker's omega pore.

248 Interestingly, both mutations also abolished Shaker's sensitivity to 4-aminopyridine, which is a phar

249 lines carrying loss-of-function mutations in Shaker (Sh) are short sleeping, suggesting that the Sh c

250 egulating the levels and open probability of Shaker (Sh) potassium channels to suppress neuronal exci

251 For example, the effects of mutations in Shaker (Sh), which encodes a K+ channel subunit, are sup

252 One such gene is Shaker (Sh), which encodes a voltage-dependent fast K(+)

253 of four functionally distinct gene families (Shaker, Shab, Shal, and Shaw) that share a subunit struc

254 icated that the characteristic properties of Shaker, Shab, Shal, Shaw, and KCNQ currents evolved befo

255 HmK is potent but promiscuous, blocking KcsA-Shaker, Shaker, Kv1.2, and Kv1.3 channels with Ki of 1-4

256 SSS and Shaker shared similar expression patterns in the brain a

257 structural constraints derived from eag and Shaker specify the unique packing arrangement of transme

258 -/- and OT+/+ male mice that were exposed to shaker stress or other stressors (i.e., administration o

259 In support of this, putative ctenophore Shaker subfamily channel subunits coassembled with cnida

260 Phylogenetic analysis suggested that the Shaker subfamily could predate the divergence of ctenoph

261 ed the function of 18 members of the 20 gene Shaker subfamily in Nematostella.

262 is present in multiple other members of the Shaker subfamily of K(+) channels and in several other u

263 notype have not previously been found in the Shaker subfamily, but have evolved independently in the

264 contrast to results previously obtained with Shaker, substitution of the tyrosine at Kv2.1 position 3

265 We traced the origin of this unique Shaker subunit structure to a common ancestor of ctenoph

266 ubunits coassembled with cnidarian and mouse Shaker subunits, but not with cnidarian Shab, Shal, or S

267 er of two Arabidopsis (Arabidopsis thaliana) Shaker subunits, K(+) channel in Arabidopsis thaliana2 (

268 a by forming heteromeric channels with other Shaker subunits.

269 currents and was co-immunoprecipitated with Shaker, suggesting that SSS modulates Shaker activity vi

270 intersubunit Zn2+ ion that is lacking in the Shaker T1 domain.

271 id side chains at the position equivalent to Shaker T449, and that TEA prevents a constriction that u

272 yrosine point mutation (K532Y, equivalent to Shaker T449Y) that diminishes C-type inactivation.

273 placed into suspension on a rotating orbital shaker to create human cardiac tissue patches.

274 annel activity is important, in concert with Shaker, to ensure proper AP repolarization.

275 ty and BrdUrd incorporation over vector- and Shaker-transfected controls.

276 Disruption of the equivalent interaction in Shaker (Trp-434-Asp-447) and Kv1.2 (Trp-366-Asp-379) lea

277 study shares some features with that of the shaker-TRP superfamily of ion channels.

278 ession of either the BK channel SLO-1 or the Shaker type potassium channel SHK-1.

279 Autoantibodies to Shaker-type (Kv1) K+ channels are now known to be associ

280 e high-affinity transporter, AtHAK5, and the Shaker-type channel, AtAKT1.

281 ts, and lynx1 can form stable complexes with Shaker-type channels and nAChRs.

282 minum block as a common feature of the plant shaker-type channels and provided evidence that aluminum

283 pendent and -independent activation of plant shaker-type channels such as SKOR, an outward rectifying

284 The voltage-gated, Shaker-type K(+) (K(V)1) channel is one key binding part

285 protein that associates with voltage-gated, Shaker-type K(+) (KV1) channels and promotes the express

286 ibodies to mature surface membrane-expressed Shaker-type K+ channels cause acquired neuromyotonia, Mo

287 A prominent regulatory property of plant shaker-type K+ channels is the 'rundown' that causes cha

288 on in voltage-gated ion channels such as the Shaker-type KV channels, a multiscale physical model is

289 activation kinetics up to 6-fold faster than Shaker-type Kv channels.

290 Shaker-type Kv1.2 channels, normally located distally to

291 d sodium channels at the node of Ranvier and Shaker-type potassium channel (Kv1.2) at the juxtaparano

292 channels within the nodal membrane, with the Shaker-type potassium channel K(v)1.2 segregated within

293 erpolarization- and depolarization-activated Shaker-type potassium channels, CLC chloride transporter

294 stigated the composition and distribution of shaker-type-potassium channels (Kv1 channels) within the

295 unnatural amino acid was incorporated in the Shaker voltage-gated potassium channel at key regions th

296 In myelinated axons, Kv1 (Shaker) voltage-gated potassium (Kv) channels are cluste

297 g a robotic model frog and an electrodynamic shaker, we demonstrate that plant-borne vibrations gener

298 age-sensitive K(+) channels such as HERG and Shaker, we found that elevated extracellular [K(+)] modu

299 nd a C-terminal deletion (Delta C) mutant of Shaker were determined by electron microscopy and single

300 Shaker, which encodes a voltage-dependent potassium chan