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 expression including enhanced slo, Shab, and Shaker.

6 elucidates the electric field profile within Shaker.

7 nctive difference between these channels 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 d with Shaker, suggesting that SSS modulates Shaker activity via a direct interaction.

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

22 which is in line with recent estimates from Shaker and Greenhawt(2) .

23 esponse of the homologous T to A mutation in Shaker and hKv1.5 channels that display C-type inactivat

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

42 s tested in (0.9% w/v NaCl) media in a water shaker bath at 37 degrees C for over 2 years.

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

44 ype 1 potassium (K(V)1) channels K(V)1.5 and Shaker, but not the related K(V)2-, K(V)4-, or K(V)7-typ

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

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

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

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

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

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

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

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

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

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

55 functional data, suggests that KvAP and the Shaker channel, to which KvAP is most often compared, pr

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

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

58 nsmembrane and extracellular portions of the Shaker channel.

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

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

61 Shaker channels control the basal level of release, indi

62 Shaker channels have provided a powerful tool to establi

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

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

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

66 Using tandem dimers of Shaker channels we show functional data distinguishing V

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

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

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

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

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

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

73 five different liquid media under static and shaker condition at different cultivation days.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

90 Comparison of Shaker family gene complements from diverse metazoan spe

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

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

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

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

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

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

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

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

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

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

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

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

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

104 ondrogenic induction culture using a see-saw shaker for 17 days.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

121 Thus, ShaKer is well placed to enable experiment-driven, trans

122 Shaker-iVSD also displays pronounced 'relaxation'.

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

124 Shaker-iVSD showed significantly altered gating kinetics

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

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

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

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

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

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

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

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

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

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

135 ilicity) and analyzed their ability to block Shaker K(+) channel under different voltage and pH condi

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

163 hat AHA can be readily incorporated into the Shaker Kv channel in place of methionine residues and mo

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

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

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

167 we were able to site-specifically label the Shaker Kv channel with two different fluorophores simult

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

186 rovide evidence that Hip14 palmitoylates the Shaker-like K(+) voltage-gated channel subunit (Kv1.1),

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

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

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

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

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

192 Shaker-like VGKC show domain-swapped configuration: VSD

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

209 We can show that Shaker outperforms its competitors and is able to predic

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

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

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

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

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

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

216 roscopy to characterize the VSD derived from Shaker potassium channel in 1-palmitoyl-2-hydroxy-sn-gly

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

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

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

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

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

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

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

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

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

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

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

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

229 uire a manually curated reference structure, ShaKer predicts reactivity data based on sequence input

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

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

232 his therapeutic strategy in the Wistar Furth shaker rat model of Purkinje cell loss resulting in trem

233 We implanted shaker rats with stimulating electrodes targeted to the

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

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

236 covalent linkage of members of the mammalian Shaker-related K(v)1 family to K(v)1.2 and systematic as

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

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

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

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

241 r bound to the oxidoreductase domain(8,9) of Shaker's K(V)beta subunit, Hyperkinetic(10,11).

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

262 a by forming heteromeric channels with other Shaker subunits.

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

264 g, whereas increased A-type currents through Shaker support tonic firing during sleep(5).

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

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

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

268 We present ShaKer to predict SHAPE data for RNA using a graph-kerne

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

290 After opening, the Shaker voltage-gated potassium (K(V)) channel rapidly in

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

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

293 ess, there are clear differences between the Shaker-VSD and Kv1.2/2.1 chimera in the S2-S3 linker and

294 anization of secondary structure elements in Shaker-VSD appears to more closely resemble the KvAP-VSD

295 Our results suggest that the Shaker-VSD in LPPG micelles is in a native-like fold and

296 obtained from shift (TALOS+) showed that the Shaker-VSD shares many structural features with the homo

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 Shaker, which encodes a voltage-dependent potassium chan

300 speculate a conserved residue in S5 (S412 in Shaker), within van der Waals distance from next subunit