ライフサイエンスコーパス: K( ) channel

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

18 1.2/1.3, Kv7.4, hERG, or inwardly rectifying K(+) channels.

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

20 sitive low-threshold voltage-activated (LVA) K(+) channels.

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

22 explanation for the high throughput rates of K(+) channels.

23 locker of small conductance Ca(2+)-activated K(+) channels.

24 res is supported by at least three groups of K(+) channels.

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

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

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

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

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

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

31 ibe the construction of a blue-light-induced K(+) channel 1 (BLINK1) engineered by fusing the plant L

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

47 dent activation of the renal outer medullary K(+) channel and ENaC, to which angiotensin II may contr

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

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

50 evels that are ten times those of most other K(+) channels and gating sensitivity to intracellular Na

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

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

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

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

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

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

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

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

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

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

61 We discuss the possible role of SR K(+) channels and, in parallel, detail the known biochem

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

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

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

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

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

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

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

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

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

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

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

73 KV11.1 voltage-gated K(+) channels are noted for unusually slow activation, f

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

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

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

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

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

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

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

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

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

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

84 ngs identify a critical role for presynaptic K(+) channels at the pinceau in ephaptic control over th

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

86 ia-susceptibility genes, including the KCNE2 K(+) channel beta subunit, are expressed in multiple tis

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

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

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

90 K(+)-channel block potentiates the AF-selective anti-AF

91 We tested the hypothesis that adding K(+)-channel blockade improves the atrium-selective elec

92 5 Pf clones, low inhibitory activity in hERG K(+) channel blockage testing, negativity in the Ames te

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

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

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

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

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

98 2+) or a combination of two Ca(2+)-activated K(+) channel blockers (iberiotoxin, 100 nm and apamin, 1

99 ated 40 of 42 silenced genes associated with K(+) channels but also normalized 638 genes down- or upr

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

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

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

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

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

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

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

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

108 sea urchin sperm, a cyclic nucleotide-gated K(+) channel (CNGK) mediates a cGMP-induced hyperpolariz

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

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

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

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

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

114 Our results indicate that, similar to SLO1 K(+) channels, cSrc blockers significantly decreased SLO

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

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

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

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

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

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

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

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

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

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

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

126 (2+)-dependent KCa3.1 are the most prevalent K(+) channels expressed by human and rat T cells.

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

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

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

130 with amebiasis that demonstrated suppressed K(+) channel expression.

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

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

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

134 The K(+) channel from Streptomyces lividians (KcsA) undergoe

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

179 The identified K(+) channels involved in the electrogenic transport wer

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

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

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

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

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

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

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

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

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

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

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

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

192 The Ca(2+)-dependent K(+) channel, KCa3.1 (KCNN4/IK/SK4), is widely expressed

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

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

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

196 alpha photosensory module to the small viral K(+) channel Kcv.

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

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

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

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

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

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

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

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

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

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

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

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

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

210 881G>A, p.R294H), encoding the voltage-gated K(+) -channel, KV 1.2, in two unrelated families with HS

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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 coding G9a in DRG neurons completely blocked K(+) channel silencing and chronic pain development afte

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

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

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

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

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

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

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

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

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

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

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

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

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

265 .3 (KCNQ3) genes, encoding for voltage-gated K(+) channel subunits underlying the neuronal M-current,

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

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

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

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

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

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

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

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

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

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

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

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

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

279 els (KCa2/3) are Ca(2+)/calmodulin regulated K(+) channels that produce membrane hyperpolarization an

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

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

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

283 he Shaker and KCNQ families of voltage-gated K(+) channels to better understand how neuronal excitabi

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 in which a subset of plant SNAREs commandeer K(+) channel VSDs to coordinate membrane trafficking wit

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

294 4 subunit was absent, whereas the density of K(+) channels was increased at the heminode.

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

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

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

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

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