ライフサイエンスコーパス: K channel

1 ls by activation of voltage and Ca(2+) gated K channels.

2 ur through two distinct pathways, the D- and K-channels.

3 ur through two distinct pathways, the D- and K-channels.

4 modulation of swimming via the opening of a K(+) channel.

5 resistance, suggesting that dopamine opens a K(+) channel.

6 hat ZxAKT1 functions as an inward-rectifying K(+) channel.

7 s and H(+)-ATPase and with the tonoplast TPK K(+) channel.

8 yperpolarization through activation of TREK2 K(+) channels.

9 rsies and challenges on the topic of cardiac K(+) channels.

10 r may be a universal gating mechanism within K(+) channels.

11 ies is also regulated by inwardly rectifying K(+) channels.

12 and movement via regulated diffusion through K(+) channels.

13 t inhibitory control of voltage-gated A-type K(+) channels.

14 ing, with most studies involving prokaryotic K(+) channels.

15 flux assay (LFA) that is applicable to most K(+) channels.

16 s express genes encoding inwardly rectifying K(+) channels.

17 and modulate the properties of voltage-gated K(+) channels.

18 prokaryotic 'inward rectifier' subfamily of K(+) channels.

19 erneurons also depend on BK Ca(2+)-activated K(+) channels.

20 domain that closely resembles voltage-gated K(+) channels.

21 y that selectively targets inward-rectifying K(+) channels.

22 1.2/1.3, Kv7.4, hERG, or inwardly rectifying K(+) channels.

23 this unexplored class of inwardly rectifying K(+) channels.

24 ed paranodal junctions, and mislocalized Kv1 K(+) channels.

25 ia the ONOO(-)-mediated inhibition of Kv11.1 K(+) channels.

26 xiliary subunits can also regulate other Slo K(+) channels.

27 letely different fold from that of canonical K(+) channels.

28 and modulate the properties of voltage-gated K(+) channels.

29 t is abrogated by blocking Ca(2+) -sensitive K(+) channels.

30 Twik-related K(+) channel 1 (TREK1), TREK2, and Twik-related arachido

31 l delayed rectifier-like human ether a-go-go K+ channel 1 (hEAG1); the effects were exacerbated for f

32 (+/-) atria, and TWIK-related acid-sensitive K(+) channel 2 (TASK-2) gene and protein expression were

33 K(+) channels, a superfamily of approximately 80 members

34 tact with E. histolytica parasites triggered K(+) channel activation and K(+) efflux by intestinal ep

35 hibitory action at the GHRH neuron level via K(+) channel activation, followed by a delayed, sst1/sst

36 predicted with VPD unexpected alterations in K(+) channel activities and changes in stomatal conducta

37 ignalling with K(+) nutrition and guard cell K(+) channel activities have not been fully explored in

38 Gates that control K(+) channel activity were found both at an intracellula

39 gene variant, supporting the hypothesis that K(+) channels affect the metabolic responses of fat cell

40 The inward-rectifying K(+) channel AKT1 constitutes an important pathway for K

41 O3(-) transporter, NPF6;3, and activates the K(+) channel AKT1, inhibits ammonium transport and modul

42 nuation of plateau depolarizations by axonal K(+) channels, allowing full axon repolarization and Na(

43 Gastrocnemius K(+) channel alpha subunit remodeling arising from Kcne3

44 Multiple K(+) channel alpha-subunits that coassemble with Hk, inc

45 sma membrane also binds with, and regulates, K(+) channels already present at the plasma membrane to

46 ypical voltage-dependent proteins, the Kv1.2 K(+) channel and the voltage sensor of the Ciona intesti

47 Drugs that block K(+) channels and gap junctions or that activate Ca(++)

48 d 32d, elicited only weak inhibition of hERG K(+) channels and hNaV1.5 Na(+) channels, and no effects

49 ed small molecule screens on three different K(+) channels and identified new activators and inhibito

50 nt function in transcriptional repression of K(+) channels and in acute-to-chronic pain transition af

51 of voltage-gated neuronal M-type (KCNQ, Kv7) K(+) channels and L-type CaV 1 Ca(2+) channels, on both

52 equence homology to the canonical tetrameric K(+) channels and lacks the TVGYG selectivity filter mot

53 The theme of the 2016 symposium was 'K(+) channels and regulation', and the objectives of the

54 The theme of the 2016 symposium was 'K(+) Channels and Regulation'.

55 tivity of large-conductance Ca(2+)-activated K(+) channels and the expression of MaxiKalpha was decre

56 In voltage-gated K(+) channels and the prokaryotic KcsA channel, conducti

57 solute uptake via physical interactions with K(+) channels and to moderate their gating at the plasma

58 hyperpolarized via activation of potassium (K(+)) channels and resultant K(+) efflux.

59 KCNK3 encodes an outward rectifier K(+) channel, and each identified mutation leads to a lo

60 physiological connections between the NALCN, K(+) channels, and gap junctions that mediate regulation

61 and indirect effects on ENaC, distal nephron K(+) channels, and WNK signaling.

62 KEY POINTS: Repolarizing currents through K(+) channels are essential for proper sinoatrial node (

63 Voltage-gated ether a go-go (EAG) K(+) channels are expressed in various types of cancer c

64 d small-conductance (KCa2) calcium-activated K(+) channels are gated by calcium binding to calmodulin

65 We concluded that K(+) channels are host mediators of amebic cytotoxicity

66 Two-pore domain (K2P) K(+) channels are major regulators of excitability that

67 Na(+)-activated K(+) channels are members of the Slo family of large con

68 K(+) channels are membrane proteins that selectively con

69 s also are consistent with the idea that the K(+) channels are nucleation points for SNARE complex as

70 outward currents through inwardly rectifying K(+) channels are reduced at more depolarized potentials

71 Sperm-specific SLO3 K(+) channels are responsible for these membrane potenti

72 Potassium (K(+)) channels are crucial for determining the shape, du

73 Potassium (K(+)) channels are membrane proteins expressed in most l

74 otransmitter-gated ion channels and two-pore K+ channels are key players in the mechanism of anesthes

75 +) channel in health and disease, as well as K(+) channels as therapeutic targets, were contributed b

76 Therefore, we envision the K-channel as a versatile, easy to use microfluidic compo

77 ctures of Slo2.2, a neuronal Na(+)-activated K(+) channel, as a function of the Na(+) concentration.

78 e-gated Ca(2+) channels and various types of K(+) channels, as well as amongst those that regulate ac

79 nct receptor subtypes coupled with different K(+) channels, astrocyte-derived ATP differentially modu

80 the human ether-a-go-go-related gene (HERG) K(+) channel at the extracellular pore (E-pore) region,

81 ction can lead to arrhythmias, and discusses K(+) channel-based therapeutics.

82 redox sensor of the voltage-gated potassium (K(+)) channel beta-subunit (Kvbeta) Hyperkinetic (Hk).

83 e of the large-conductance Ca(2+) -activated K(+) channel (BK) and voltage-dependent K(+) channels (K

84 dium channel (ENaC) and the Ca(2+)-activated K(+) channel BKCa.

85 Eventually, hERG K-channel block was identified as the main limitation of

86 5 Pf clones, low inhibitory activity in hERG K(+) channel blockage testing, negativity in the Ames te

87 The K(+) channel blocker Ba(2+) blocks both the CSD- and the

88 The K(+) channel blocker barium chloride (but not TEA, glybe

89 most potent, the EPA approved Hybrid (Ca(++)/K(+) channel blocker), was studied for pre-lethal effect

90 illine, a large-conductance Ca(2+)-activated K(+) channel blocker, and by 4-aminopyridine, a voltage-

91 illine, a large-conductance Ca(2+)-activated K(+) channel blocker, and by 4-aminopyridine, a voltage-

92 4-aminopyridine or related voltage-dependent K channel blockers could be a useful additional therapeu

93 set of SNAREs that interact to control these K(+) channels, but with opposing actions on gating.

94 the human ether-a-go-go-related gene (HERG) K(+) channel by inhibiting the corresponding current, IK

95 Inhibition of human K(+) channels by genetic silencing, pharmacologic inhibi

96 f human ether-a-go-go-related gene 1 (hERG1) K(+) channels by many drugs delays cardiac repolarizatio

97 her the cell death-enabling function of this K(+) channel can be selectively targeted to improve neur

98 Broadly speaking, K(+) channels can be classified based on whether their m

99 dy indicates that inhibition of these A-type K(+) channels can restore the intrinsic excitability pro

100 the structure of a complete Na(+)-activated K(+) channel, chicken Slo2.2, in the Na(+)-free state, d

101 K(+) channels commonly possess two pore gates, one at th

102 Outwardly rectifying K(+) channels conduct greater current at depolarized mem

103 st experimental evidence that oxidation of a K(+) channel constitutes a mechanism of neuronal and cog

104 K(+) channels containing Kv1.1 alpha subunits, which bec

105 mediated by Ether-a-go-go-Related Gene (ERG) K(+) channels contributes to persistent firing in neocor

106 A similar K(+) channel dependence was identified for other bunyavi

107 ed as the K(+) channel family mediating BUNV K(+) channel dependence.

108 ger insulin release by closing ATP-sensitive K+ channels, depolarizing beta cells, and opening voltag

109 genetic tools lacks a light-gated potassium (K(+)) channel desirable for silencing of excitable cells

110 Notably, expression of the ROMK K(+) channel did not change in the distal convoluted tub

111 KCNE3 was the first reported skeletal muscle K(+) channel disease gene, but the requirement for KCNE3

112 (+), Cl(-) cotransporter (NKCC) and the Shaw K(+) channel (dKV3.1).

113 gnificant homology with the highly selective K(+) channels, do not discriminate among monovalent alka

114 pproach is used to quantify ion binding to a K(+) channel embedded in bicelles and can be applied to

115 treatment of cells expressing voltage-gated K(+) channels enabled the visualization of intracellular

116 l for injection (after the droplet splitting K-channel) enables integrated washing of magnetic beads

117 e two-pore domain channel THIK-1 as the main K(+) channel expressed in microglia in situ.

118 imination of TASK-2 (K(2P)5), a pH-sensitive K(+) channel expressed in RTN neurons, essentially aboli

119 (2+)-dependent KCa3.1 are the most prevalent K(+) channels expressed by human and rat T cells.

120 rgent and persistent Na(+) currents, whereas K(+) channel expression and currents were increased.

121 ve injury causes a long-lasting reduction in K(+) channel expression in the dorsal root ganglion (DRG

122 ut only G9a inhibition consistently restored K(+) channel expression.

123 KCNQ (voltage-gated K(+) channel family 7 (Kv7)) channels control cellular e

124 n K(+) channels (K2P) were identified as the K(+) channel family mediating BUNV K(+) channel dependen

125 rs to be distinct from that of the classical K(+) channel family.

126 Addition of a second K-channel for injection (after the droplet splitting K-c

127 A back-door strategy is to use KcsA (a K(+) channel from the bacteria Streptomyces lividans) as

128 tic cycle, where proton transfer through the K-channel, from K362 to Y288 at the BNC, is important.

129 that these biophysical changes in Na(+) and K(+) channel function could reliably reproduce the obser

130 channel modulating agents demonstrated that K(+) channel function is critical to events shortly afte

131 surprising that essentially every aspect of K(+) channel function is exquisitely regulated in cardia

132 ium on the structural basis of voltage-gated K(+) channel function, as well as the mechanisms involve

133 uxiliary subunits are often needed to tailor K(+) channel functional properties and expression levels

134 unit of C. elegans SLO-2, a high-conductance K(+) channel gated by membrane voltage and cytosolic Cl(

135 ified for mammalian Slo1, a high-conductance K(+) channel gated by voltage and Ca(2+).

136 bsequently with SYP121, thereby coordinating K(+) channel gating during SNARE assembly and vesicle fu

137 as the mechanisms involved in regulation of K(+) channel gating, expression and membrane localizatio

138 ions and were associated with alterations in K(+) channel gating.

139 ree other members of the ether-a-go-go (EAG) K(+) channel gene family, including EAG1 (Kv10.1), ERG3

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

141 hanced activation of the G-protein-activated K(+) channel (GIRK; Kir3.1/Kir3.4) was shown when mutant

142 tion of the gate that opens Ca(2+)-activated K(+) channels has remained elusive.

143 Two modes of gating present in other K(+) channels have been considered.

144 ne expression of the human voltage-dependent K(+) channel human ether-a-go-go-related gene (hERG) in

145 recent report suggested the Ca(2+)-activated K(+) channel, IK1 (KCNN4) as the sAHP channel in CA1 pyr

146 cological inhibition of the muscarinic-gated K(+) channel (IKACh) could rescue SSS and heart block in

147 The rapidly activating delayed rectifier K(+) channel (IKr) is encoded by the human ether-a-go-go

148 TREK-2 is a mammalian two-pore domain (K2P) K(+) channel important for mechanosensation, and recent

149 sembles with the alpha-subunit KCNQ1 to form K(+) channels important for K(+) and Cl(-) secretion tha

150 ed upregulation of the renal outer medullary K(+) channel in AS(-/-) mice, whereas upregulation of th

151 using on the functional roles of the cardiac K(+) channel in health and disease, as well as K(+) chan

152 We identify KIR2.1 as the acid-sensitive K(+) channel in sour taste cells using pharmacological a

153 KCNE2 may regulate multiple K(+) channels in beta cells, including the T2DM-linked K

154 -mediated inhibition of cardiac ERG (Kv11.1) K(+) channels in carbon monoxide-induced proarrhythmic e

155 ing paper focuses on the integrative role of K(+) channels in cardiac electrophysiology, i.e. how K(+

156 Given the critical role for K(+) channels in determining the rate of cardiac repolar

157 at regulates the activity of Na(+)-activated K(+) channels in neurons.SIGNIFICANCE STATEMENT Slack Na

158 at H2O2-elicited dilation involves different K(+) channels in non-CAD versus CAD, resulting in an alt

159 roversies on the functional roles of cardiac K(+) channels in normal and diseased heart.

160 ation of small conductance calcium-activated K(+) channels in PDGFRalpha(+) cells, and the excitatory

161 ctivating large-conductance Ca(2+)-activated K(+) channels in subjects with coronary artery disease (

162 ids, resemble the pore module of all complex K(+) channels in terms of structure and function.

163 evidence for the essential participation of K(+) channels in the electrogenic transport of human ES

164 uman ES and investigated the contribution of K(+) channels in the electrogenic transport, which has b

165 m K(+) channels that are voltage-independent K(+) channels in the physiological voltage range and imp

166 TRPs, leak K(+) and voltage-gated Na(+) and K(+) channels in the transduction of cold by nociceptors

167 d mRNA levels for the SK3 subunit of SK-type K(+) channels in ventral pyramidal cells is associated w

168 It is known that potassium (K(+)) channels in the ventral tegmental area (VTA) are a

169 l attributes that differ from those of other K(+) channels, including a dimeric assembly constituted

170 Our data suggest that voltage-dependent K+ channel inhibition with 4-aminopyridine treatment res

171 ubunits and two types of auxiliary subunits: K(+) channel-interacting proteins (KChIPs) and dipeptidy

172 mplexes including pore-forming Kv4 subunits, K(+) channel-interacting proteins (KChIPs), and dipeptid

173 vertheless, the localization and role of ClC-K channels is not fully resolved.

174 The gate in Slo1 K(+) channels is regulated by two separate stimuli, intr

175 embrane protein 175 (TMEM175), the lysosomal K(+) channel, is centered under a major genome-wide asso

176 balance hypokalaemia-induced two pore-domain K(+) channel isoform 1 (K2P1) leak cation currents, reco

177 s with ectopic expression of two pore-domain K(+) channel isoform 1 (K2P1) recapitulate two levels of

178 , namely, small and intermediate conductance K(+) channels (K(Ca)3.1 and K(Ca)2.3) and endothelial ni

179 nnel (TREK-1) belongs to the two-pore domain K(+) channels (K2P) and displays various properties incl

180 cological screening regimen, two-pore domain K(+) channels (K2P) were identified as the K(+) channel

181 However, the acetylcholine-gated K(+) channel (KACh) conducts current that inwardly recti

182 ress the activities of the inward-rectifying K(+) channels KAT1 and KC1.

183 tidine phosphorylation and activation of the K(+) channel KCa3.1, which is required for TCR-stimulate

184 nvolves the activity of the Ca(2+)-activated K(+) channel KCa3.1.

185 he intermediate-conductance Ca(2+)-activated K(+) channel (KCa3.1) constitutes an attractive pharmaco

186 The delayed rectifier potassium (K(+)) channel KCNB1 (Kv2.1), which conducts a major soma

187 The K(+) channel KCNQ1 has been proposed as a tumor suppress

188 SIGNIFICANCE STATEMENT Slack Na(+)-activated K(+) channels (KCNT1, KNa1.1) regulate neuronal excitabi

189 ental and computational analysis between two K(+) channels, KcvS and KcvNTS.

190 nd enhanced block of the inwardly rectifying K(+) channel Kir2.1, compared with the wild-type sigma-1

191 ression of gene transcripts, G-protein gated K(+) channel (Kir3) and KATP (Kir6) currents were not re

192 gh downregulation of the inwardly rectifying K(+) channel Kir4.1 in satellite glial cells.

193 gh downregulation of the inwardly rectifying K(+) channel Kir4.1 in satellite glial cells.

194 tivation of Src kinase, up-regulation of the K(+) channel Kir4.1, and stimulation of the Cl(-) channe

195 he KCNJ15 gene (encoding inwardly rectifying K(+) channel Kir4.2) specifically abolishes galvanotaxis

196 BC transporter SUR1 and the inward-rectifier K(+) channel Kir6.2, in the presence of Mg(2+) and nucle

197 Compared to the Ca(2+)-activated K(+) channels, known as BK and SK channels, the physiolo

198 Adcy10 (soluble adenylyl cyclase) and Slo3 (K(+) channel) KO mice.

199 uctance KCa (BK) and other voltage-dependent K(+) channels (Kv) are highly expressed in carotid body

200 Voltage-gated K(+) channels (Kv) are responsible for repolarizing exci

201 ated K(+) channel (BK) and voltage-dependent K(+) channels (Kv) on [Ca(2+) ]i responses to a wide ran

202 881G>A, p.R294H), encoding the voltage-gated K(+) -channel, KV 1.2, in two unrelated families with HS

203 n or a gain-of-function of the voltage-gated K+ channel Kv1.2, were described to cause a new molecula

204 by decreasing activity of voltage-dependent K channels (Kv1.3).

205 The voltage-gated K(+) channel Kv2.1 has been intimately linked with neuro

206 The voltage-gated K(+) channels Kv7.2 and Kv7.3 are located at the axon in

207 The voltage-gated K(+) channels Kv7.2 and Kv7.3 exert strong control over

208 On the other hand, numerous ligand-gated K(+) channels lack such gate, suggesting that they may b

209 In the K(+) channel-like transmembrane domain, Ca(2+) selectivi

210 necessary signal for the modulation of Kv2.1 K(+) channel localization and physiological function.

211 M-type K(+) channels (M-channels), important regulators of neur

212 are visibly distinct from closing events in K(+) channels makes unambiguous interpretation of data f

213 pendent mechanism, whereas Ca(2+) -sensitive K(+) channels mediate FIV via an NO-independent pathway.

214 f human ether-a-go-go-related gene 1 (hERG1) K(+) channels mediates repolarization of action potentia

215 Time of addition assays using K(+) channel modulating agents demonstrated that K(+) ch

216 This study is the first to show that K(+) channel modulatory subunits KChIP1, KChIP2, and DPP

217 he Kv4 complex, this study demonstrates that K(+) channel modulatory subunits KChIP1, KChIP2, and DPP

218 K(+) channel modulatory subunits KChIP1, KChIP2, and DPP

219 unit structure consisting of a voltage-gated K(+) channel motif coupled to a cytoplasmic domain that

220 hat a major diversification of voltage-gated K(+) channels occurred in ancestral parahoxozoans and im

221 C-type inactivation in most K(+) channels occurs upon sustained membrane depolarizat

222 Reportedly, voltage and Ca(2+)-activated K(+) channels of the BK type are stimulated by cGMP/cGMP

223 tion of current carried by inward-rectifying K(+) channels of tobacco (Nicotiana tabacum) guard cells

224 the D- and K-channel, show the impact of the K-channel on the D-channel to be protonation-state depen

225 odel of depression, we report that KCNQ-type K(+) channel openers, including FDA-approved drug retiga

226 gh enhanced expression of Kv4.2/Kv4.3 A-type K(+) channels, particularly within the cell bodies of CA

227 unction and expression of Kv4.2/Kv4.3 A-type K(+) channels, particularly within the perisomatic compa

228 enium complexes suggested that ATP-sensitive K(+) channel pathways were not involved because glibencl

229 K-channels perform reagent injection (0-100% of droplet

230 because they form a channel complex with the K(+) channel pore-forming subunit Kv4.3 in a subset of n

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

232 of activation and inactivation gates of the K(+) channel pore.

233 endothelial cells lack the Ca(2+) -activated K(+) channels present in arterial endothelium to generat

234 ied pressure and electric field, selects the K-channel process and tunes its magnitude.

235 In many K(+) channels, prolonged activating stimuli lead to a ti

236 These small viral encoded K(+) channel proteins, with a monomer size of only 82 am

237 Ultimately, the K-channel provides an exciting opportunity to perform ma

238 e eukaryotic and most bacterial ligand-gated K(+) channels, RCK domains regulate ion fluxes.

239 betes, we found that activation of the TRESK K(+) channel reduced NG excitability and disrupted gastr

240 K(+) channel regulatory mechanisms alter, and are altere

241 A fundamental understanding of K(+) channel regulatory mechanisms and disease processes

242 rk, change with the protonation state of the K-channel residue K362.

243 work depends on the protonation state of the K-channel residue K362.

244 Reducing expression of the TRESK K(+) channel restored NG excitability in vitro and in vi

245 hods to determine how Kv3.4, a voltage-gated K(+) channel robustly expressed in dorsal root ganglion

246 However, uncoupling the Shaker K(+) channel's pore domain (PD) from the VSD prevented t

247 exity of the conformational landscape of the K(+) channel selectivity filter and its dependence on th

248 HCN channels contain a K(+) channel selectivity filter-forming sequence from wh

249 ansmembrane-spanning segments and has no GYG K(+) channel sequence signature-containing, pore-forming

250 ss filtering of dendritic plateaus by axonal K(+) channels should thus enable accurate transmission o

251 onation states of key residues in the D- and K-channel show the mutual impact of the two proton-condu

252 onation states of key residues in the D- and K-channel, show the impact of the K-channel on the D-cha

253 The small conductance K channel (SK) activity showed no difference of channel

254 BSTRACT: Small conductance Ca(2+) -activated K(+) channels (SK) play an important role in regulating

255 Small-conductance, Ca(2+) -activated K(+) channels (SK, KCa 2) are expressed in human atrial

256 Small-conductance, Ca(2+) -activated K(+) channels (SK, KCa 2) are unique subclasses of K(+)

257 x is negatively regulated by Ca2+ -activated K+ channels (SK-channels) which are in turn inhibited by

258 wo members of the family of high conductance K(+)channels SLO1 and SLO2 are both activated by intrace

259 The Ca(2+)-activated K(+) channel, Slo1, has an unusually large conductance a

260 Inward rectifier K(+) channel subfamily 2 (Kir2) channels primarily maint

261 ABSTRACT: Inward rectifier K(+) channel subfamily 2 (Kir2) channels primarily maint

262 present study, we show that inward rectifier K(+) channel subfamily 2 isoform 1 (Kir2.1) currents non

263 Expression of the TREK (TWIK-related K(+) channel) subfamily members of K2P channels often ov

264 Contactin-2 and Scn5a and downregulation of K(+) channel subunit genes that contribute to Ito,f and

265 binding and loss of active histone marks on K(+) channel subunit promoters with Notch activation, an

266 these non-excitable cells also requires the K(+) channel subunits Hyperkinetic, Shaker, and ether-a-

267 More than 80 genes encode the K(+) channel subunits in the human genome.

268 concomitant with altered gene expression of K(+)-channel subunits and ion channel modulators, releva

269 ion in sour taste cells of an acid-sensitive K(+) channel suggests a mechanism for amplification of s

270 f ion fluxes in LECs indicated that omitting K(+) channels supports our experimental results.

271 he expression of Twik-related acid-sensitive K(+) channel (TASK)-1 [a pH-sensitive potassium channel

272 We concluded that the K(+) channel TASK1 controls the thermogenic activity in

273 b, and KCTD16 subunits (named after their T1 K(+)-channel tetramerization domain) that regulate G-pro

274 TMEM175 is a lysosomal K(+) channel that is important for maintaining the membr

275 Therefore, we have identified a lysosomal K(+) channel that provides a positive feedback mechanism

276 Thus, TMEM175 comprises a K(+) channel that underlies the molecular mechanism of l

277 hannels (SK, KCa 2) are unique subclasses of K(+) channels that are regulated by Ca(2+) inside the ce

278 kidney, KCNE3 coassembles with KCNQ1 to form K(+) channels that are voltage-independent K(+) channels

279 mbers of the Slo family of large conductance K(+) channels that are widely expressed in the brain, wh

280 filter is an essential functional element of K(+) channels that is highly conserved both in terms of

281 are due to an enhanced activation of SK-type K(+) channels that suppresses NMDAR-dependent EPSP ampli

282 structure of the selectivity filter to other K(+) channels, the structure diverges significantly in m

283 any of the approximately 80 plasma membrane K(+) channels, TMEM175 has two repeats of 6-transmembran

284 , binds the voltage sensor domains (VSDs) of K(+) channels to confer a voltage dependence on secretor

285 ssues and reveal that CRY acts together with K(+) channels to maintain passive membrane properties in

286 V activates and requires cellular potassium (K(+)) channels to infect cells.

287 and Twik-related arachidonic-acid stimulated K(+) channel (TRAAK) form the TREK subfamily of two-pore

288 The TWIK-related K(+) channel (TREK-1) belongs to the two-pore domain K(+

289 The TWIK-related K(+) channel, TREK-1, has recently emerged as an attract

290 BK K(+) channels undergo N-type inactivation via their beta

291 to drive membrane fusion, binds to the KAT1 K(+) channel via two sites on the protein, only one of w

292 Specific inhibition of Ca(2+)-dependent K(+) channels was highly effective in preventing amebic

293 4 subunit was absent, whereas the density of K(+) channels was increased at the heminode.

294 Potassium (K(+)) channels were the most common transporter identifi

295 the HERG (human ether-a-go-go-related gene) K(+) channel, which conducts the rapidly activating dela

296 K(+) channels, which act to reduce nociceptor activity,

297 S plasticity by selectively targeting M-type K(+) channels, which predominantly localize to the AIS a

298 ng droplet chemistry, we have developed the "K-channel," which couples a cross-channel flow to the se

299 CNE3 (MiRP2) forms heteromeric voltage-gated K(+) channels with the skeletal muscle-expressed KCNC4 (

300 K2P K(+) channels with two pore domains in tandem associate