ライフサイエンスコーパス: K channel

1 IRK (G-protein activated inwardly rectifying K(+) channel).

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

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

4 lone and not the physiologically relevant I (Ks) channel.

5 tance, voltage- and Ca(2+)-dependent BK-type K(+) channel.

6 ary to the previous suggestion of it being a K(+) channel.

7 REK-1 and TWIK-related alkaline pH-activated K(+) channel.

8 nodes of Ranvier contain a mechanosensitive K(+) channel.

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

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

11 vation is not required for the opening of I (Ks) channels.

12 cy dependence of mefenamic acid action on I (Ks) channels.

13 Chinese hamster ovary cells overexpressing I(Ks) channels.

14 e that KCNQ1 antibodies act as agonists on I(Ks) channels.

15 th intrinsic pH sensitivity likely driven by K(+) channels.

16 nels (VGKCs), and Ca(2+)-activated SK and BK K(+) channels.

17 ribute to our understanding of the action of K(+) channels.

18 some of the complex functional behaviour of K(+) channels.

19 tivity and controlling the transport rate of K(+) channels.

20 diate and large conductance Ca(2+)-activated K(+) channels.

21 o types of Ca(2+) channels and four types of K(+) channels.

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

23 s express genes encoding 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 and modulate the properties of voltage-gated K(+) channels.

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

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

30 on via inhibition of the inwardly rectifying K(+) channels.

31 gets to the membrane and regulates Na(+) and K(+) channels.

32 cerevisiae (ScTOK), and distinct from other K(+) channels.

33 sm leading to Ca(2+)-dependent activation of K(+) channels.

34 for an improved understanding of eukaryotic K(+) channels.

35 is a classic permeant blocker of potassium (K(+)) channels.

36 TASK-1 (K(+) channel-related acid-sensitive K(+) channel-1) (K(2P)3.1) atrial-specific 2-pore domain

37 autoimmunity against the voltage-gated KCNQ1 K(+) channels accelerates cardiac repolarization.

38 tion of the kinetics of dendritic Ca(2+) and K(+) channels activated by CF-EPSPs, based on optical me

39 ation, suggesting that VRAC acts upstream of K(+) channel activation.

40 cover an unrecognized polypharmacology among K(+) channel activators and highlight a filter gating ma

41 K(+) channel activators had no effect on the degree of C

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

43 sparks") and corresponding Ca(2+)-activated K(+) channel activity are critically important for balan

44 alyx of Held synapse, we find that Na(+) and K(+) channels affect the timing by changing the AP wavef

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

46 n the cytosolic side of the inward-rectifier K(+) channel AKT1 regulates kinase docking and channel a

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

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

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

50 activator of TRESK [TWIK-related spinal cord K(+) channel (also known as K(2P)18.1)] background potas

51 eriments, with ALD in the presence of NKCC1, K(+) channel and mineralocorticoid receptor inhibitors,

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

53 of individual subunits in native heteromeric K(+) channels and establishing their physiological roles

54 ever, the sequence of SNARE binding with the K(+) channels and its interweaving within the events of

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

56 lular Ca(2+) signals to KCNQ (Kv7, "M-type") K(+) channels and many other ion channels.

57 ng mechanisms of EAG and related ERG and ELK K(+) channels and places the PAS domain as a new target

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

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

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

61 RCK domains regulate the activity of K(+) channels and transporters in eukaryotic and prokary

62 KCNQ (Kv7, "M-type") K(+) channels and TRPC (transient receptor potential, "c

63 decreases the voltage sensitivity of the I (Ks) channel and shifts channel gating kinetics toward mo

64 to the discovery that a clinically approved K(+) channel antagonist is able to rescue the dominant-n

65 Divergent responses to the K-channel antagonist, kappaM-conopeptide RIIIJ (RIIIJ),

66 ts, here we show that modal gating shifts in K(+) channels are associated with important changes in t

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

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

69 EAG (ether-a-go-go) family of voltage-gated K(+) channels are important regulators of neuronal and c

70 voltage-gated, two-pore domain, and related K(+) channels are located in eukaryotic membranes rich i

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

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

73 se that open the internal gates in classical K(+) channels are shown to produce inward TOK currents.

74 (2+) in the eukaryotic BK and bacterial MthK K(+) channels are well understood.

75 Potassium (K(+)) channels are highly conserved proteins found in al

76 imal toxins exposes the peripheral cavity of K(+) channels as a novel pharmacological target and prov

77 These K2P channels, but not voltage-gated K(+) channels as in other parts of nerves, are required

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

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

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

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

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

83 Of these, K(+) channel binding and its displacement of the regulat

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

85 activated large conductance Ca(2+)-activated K(+) channel (BK) current is prominent, and in mammalian

86 We expressed the synthetic, light-gated K(+) channel BLINK1 in guard cells surrounding stomatal

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

88 thod: increasing I(CaL,D-C) amplitude and/or K(+) channel-blockade (4-aminopyridine).

89 xpression of K(V)7.2 in the axons, using the K(+) channel blocker tetraethylammonium ions, we suggest

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

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

92 two subtypes of sarcoplasmic reticulum (SR) K(+) -channel but their individual functional roles are

93 endritic excitability by inactivating A-type K(+) channels, but this phenomenon is not restricted to

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

95 Mutations in KCNC3, which encodes the Kv3.3 K(+) channel, cause spinocerebellar ataxia 13 (SCA13).

96 While the mechanisms of AIS Na(+) and K(+) channel clustering are understood, the molecular me

97 Given that mefenamic acid can enhance all I (Ks) channel complexes containing different ratios of KCN

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

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

100 expression of VGCCs and Ca(2+)-dependent BK K(+) channels coupled to ACh release at the MOC-OHC syna

101 re compared the biophysical properties of SR K(+) -channels derived from the skeletal muscle of wild-

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

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

104 major role of voltage-independent potassium (K(+))-channel dysfunction in hyperexcitability of CA3 py

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

106 GEP indicated the overexpression of both the K(+) channel encoding gene KCNN4, and SLC2A1, which enco

107 A completely different profile of K(+) channel encoding genes emerged in DLBCL accompanied

108 (2+)-dependent KCa3.1 are the most prevalent K(+) channels expressed by human and rat T cells.

109 7 channels are a family of voltage-dependent K(+) channels expressed in many cell types, which open i

110 KCNJ2 K(+) channel expression in peripheral blood mononuclear

111 infections, via cytokine-mediated changes in K(+) channel expression.

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

113 It shares the common inward-rectifier K(+) channel fold with eukaryotic channels, including co

114 ining the vectorially oriented voltage-gated K(+) channel for the activated, open and deactivated, cl

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

116 We find that lone SR K(+) -channels from Tric-a KO mice have a lower open pro

117 , unlike channels from WT mice, the Po of SR K(+) -channels from Tric-a KO mice increased as increasi

118 skeletal muscle sarcoplasmic reticulum (SR) K(+) -channels from wild-type (WT) mice (where TRIC-A is

119 KirBac1.1 is a prokaryotic inward-rectifier K(+) channel from Burkholderia pseudomallei.

120 as BK channels and MthK, a Ca(2+)-activated K(+) channel from Methanobacterium thermoautotrophicum,

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

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

123 Voltage-gated K(+) channels function in macromolecular complexes with

124 vity, protein degradation, heme degradation, K+ channel function, two-component signal transduction,

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

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

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

128 ic mechanisms but act as master keys to open K(+) channels gated at their selectivity filter (SF), in

129 two gates, distinct from previously observed K(+) channel gates, controlled by stimuli on either side

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

131 gs, such as G-protein-gated inward rectifier K(+) channels (GIRK), have differential permissibility;

132 The tetrameric G protein-gated K(+) channels (GIRKs) mediate inhibitory effects of neur

133 ent studies have demonstrated that bacterial K(+) channels have integral roles in electrical signalin

134 Potassium (K(+)) channels have been evolutionarily tuned for activa

135 3) gene, which encodes an outward rectifier K(+) channel, have been identified in pulmonary arterial

136 sense mutations in KCNH1 and KCNK4, encoding K(+) channels, have been identified in subjects with ZLS

137 the pore (hKir6.2) of a human ATP-sensitive K(+) channel (hK(ATP)).

138 ation of slowly activating delayed rectifier K(+) channels (I(Ks)), suggesting important roles of I(N

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

140 minant negative for TRESK, a two-pore-domain K+ channel implicated in migraine: TRESK-MT, a 2-bp fram

141 nteraction between ryanodine receptor and SR K(+) -channels in Tric-a KO SR, suggesting that TRIC-B-T

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

143 pore-forming domain of the delayed rectifier K(+) channel in the heart.

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

145 sites where Kv2 (the major delayed rectifier K(+) channels in brain) and other PM and ER ion channels

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

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

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

149 TOKs are outwardly rectifying K(+) channels in fungi with two pore-loops and eight tra

150 osed states of three different voltage-gated K(+) channels in hydrated phospholipid bilayer membrane

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

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

153 rmous progress has been made to characterize K(+) channels in the primary auditory neurons, the molec

154 1 in arterial smooth muscle cells is to form K(+) channels in the sarcolemma.

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

156 Leiurus scorpion venom, blocks voltage-gated K(+)-channels in a unique example of binding/unbinding s

157 ilitated by higher expression of SOS1 (Na(+)/K(+) channel) in transgenic plants as compared to WT pla

158 nnels, nor did the presence or absence of SR K(+) -channels influence ryanodine receptor activity.

159 bunits, modulatory auxiliary subunits called K(+) channel-interacting proteins (KChIPs) modulate Kv4

160 m underlying the voltage-dependent gating of K channels is usually addressed theoretically using mole

161 TRESK (K2P18.1) background K(+) channel is a major determinant of the excitability

162 hERG K(+) channel is important for controlling the duration o

163 The vast complexity of native heteromeric K(+) channels is largely unexplored.

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

165 if, located within the voltage sensor of the K(+) channels, is a nexus for multiple SNARE interaction

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

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

168 he hyperpolarization as the Ca(2+)-activated K(+) channel K(Ca)3.1.

169 ariant in KCNA2, which encodes voltage-gated K(+) channel K(V) 1.2.

170 Pancreatic ATP-sensitive K(+) channels (K(ATP)) comprise four inward rectifier su

171 The response of ATP-sensitive K(+) channels (K(ATP)) to cellular metabolism is coordin

172 Here we show that ATP-sensitive K(+) channels (K(ATP)), hugely abundant in cardiac ventr

173 of intermediate conductance Ca(2+)-activated K(+) channels (K(Ca)3.1), and direct stimulation of the

174 Loss of ATP sensitive K(+) channel (KATP) current contributes to I/R injury, a

175 The ATP-sensitive K+ channel (KATP) is formed by the association of four i

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

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

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

179 ivity filter of the prototypical full-length K(+) channel KcsA by solution state NMR spectroscopy in

180 In the K(+) channel KcsA, a multitude of fast activity shifts t

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

182 cause by overexpressing the inward rectifier K channel Kir2.1 in stabilizer cells.

183 Here we use human Inward Rectifier K(+) Channel Kir2.1 to map site-specific permissibility

184 Using the Inward Rectifier K+ channel Kir2.1, we validate the practical utility of

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

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

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

188 ion of the glial-specific, inward-rectifying K(+) channel Kir4.1.

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

190 the association of four inwardly rectifying K+ channel (Kir6.x) pore subunits with four sulphonylure

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

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

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

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

195 nteraction between DAT and the voltage-gated K(+) channel Kv2.1 (potassium voltage-gated channel subf

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

197 The voltage-gated K(+) channel Kv2.1 serves a major structural role in the

198 s, K(ATP) (Kir6) channels, voltage-dependent K channels (Kv4, Kv7, and Kv11), twin-pore domain K chan

199 a PUFA analogue selective for the cardiac I(Ks) channel (Kv7.1/KCNE1) is effective in shortening the

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

201 Moreover, A-type K(+) channels limit the activation of P/Q-type Ca(2+) ch

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

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

204 ealed interactions between NKCC1 and outward K(+) channels, mediated by a mineralocorticoid receptor-

205 potency of kappaM-RIIIJ block of heteromeric K(+) channel-mediated currents in heterologous expressio

206 CNK9) channels, a subtype of two-pore domain K(+) channels, mimicked the SF effects by increasing the

207 , AP shortening induced by activators of two K(+) channels (ML277 for Kv7.1 and NS1643 for Kv11.1) ab

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

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

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

211 des de Pointes; (3) the relationship between K(+) channel mRNA levels in ventricles and peripheral bl

212 he nodes of Ranvier have clustered Na(+) and K(+) channels necessary for rapid and efficient axonal a

213 els did not directly affect the gating of SR K(+) -channels, nor did the presence or absence of SR K(

214 Ca(2+)- and voltage-gated K(+) channels of large conductance (BK channels) are exp

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

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

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

218 In potassium (K(+)) channels, permeation, selectivity, and gating at t

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

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

221 CTX plugs the external mouth of K(+)-channels pore, stopping K(+)-ion conduction, withou

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

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

224 taining a vectorially oriented voltage-gated K(+) channel protein at high in-plane density tethered t

225 embranes were dominated by the voltage-gated K(+) channel protein because of the high in-plane densit

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

227 selectivity filter, a hallmark of all known K(+) channels, raising the question how selectivity is a

228 The Kv4 family of A-type voltage-gated K(+) channels regulates the excitability in hippocampal

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

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

231 domains in a weak inward rectifying TASK-1 (K(+) channel-related acid-sensitive K(+) channel-1) (K(2

232 Kv7 K(+) channels represent attractive pharmacological targe

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

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

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

236 ic ion-bound configurations coexist within a K(+) channel's selectivity filter, which fully agrees wi

237 water, K(+)-ion-bound configuration) of the K(+) channel's selectivity filter.

238 and suggest that the activity of yet unknown K(+) channel(s), but not TPK3, is critical for optimal p

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

240 Thus, we suggest that SYP121 binding to the K(+) channels serves the role of a primary trigger to in

241 Potassium (K(+)) channels shape the response properties of neurons.

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

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

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

245 cific knockout (KO) of the calcium-activated K+ channel SK2 (L7-SK2) show intact vestibulo-ocular ref

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

247 termediate (KCNN4) conductance, Na-activated K channels (Slo2), voltage-gated (SCN) Na(+) and Na(+) l

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

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

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

251 Voltage-gated potassium (K(+)) channel subfamily B member 1 (KCNB1, Kv2.1) and in

252 that regulates the association of the A-type K(+) channel subunit Kv4.2 with its auxiliary subunit di

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

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

255 f intracellular K(+) and the deletion of the K(+) channel suggested that the hyperpolarization respon

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

257 nnels (Kv4, Kv7, and Kv11), twin-pore domain K channels (TASK, TREK), inward rectifier Kir7.1, Ca(2+)

258 A2793 inhibited TWIK-related acid-sensitive K(+) channel (TASK)-1 (100 uM, 53.4% +/- 13, 5%, n = 5),

259 Here, we identify the K(+) channel tetramerization domain 5 (KCTD5) protein, a

260 TRAAK is a membrane tension-activated K(+) channel that has been associated through behavioral

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

262 also known as Kv7.1, is a voltage-dependent K(+) channel that regulates gastric acid secretion, salt

263 Slo1 is a Ca(2+)- and voltage-activated K(+) channel that underlies skeletal and smooth muscle c

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

265 K(V) 7 channels are voltage-dependent K(+) channels that open in response to membrane depolari

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

267 EM175 family constitutes recently discovered K(+)channels that are important for autophagosome turnov

268 d in the cryo-EM structure of the bovine CLC-K channel, though the volume of the intracellular (inner

269 n of P/Q-type Ca(2+) channels and associated K(+) channels, thus preventing the generation of Ca(2+)

270 he test, we locked the conformation of a Kir K(+) channel to prevent widening of the narrow collar.

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

272 is known that amiodarone (AMD) acts on hERG K(+) channels to treat cardiac arrhythmias with relative

273 imental effects: for example, opening nearby K(+) channels to weaken synaptic efficacy and reduce neu

274 s TREK1 and TREK2, two other two-pore-domain K+ channels, to increase trigeminal sensory neuron excit

275 Arabidopsis (Arabidopsis thaliana) two-pore K(+) channel TPK3, which had been reported to mediate th

276 olecules that robustly activate TWIK-related K(+) channels (TREK-1) and reversibly induce loss of con

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

278 ithin potassium channels [e.g., TWIK-related K(+) channel type 1 (K2P2.1, TREK-1)].

279 dine preferentially blocks inward-rectifying K+ channel type 2 (Kir2) channels in striatal spiny proj

280 ) and analyzed their ability to block Shaker K(+) channel under different voltage and pH conditions.

281 gated Ca(2+) channels (VGCCs), voltage-gated K(+) channels (VGKCs), and Ca(2+)-activated SK and BK K(

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

283 When lone SR K(+) -channels were incorporated into bilayers, the open

284 all available high-resolution structures for K(+) channels were swept for potential binding sites.

285 sing circGORK (Guard cell outward-rectifying K(+) -channel) were hypersensitive to abscisic acid, but

286 downregulation of calcium-dependent SK-type K(+) channels, which contribute to a medium-slow afterhy

287 rive the final stages of vesicle fusion, and K(+) channels, which facilitate uptake of the cation to

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

289 dscape in a mutant that mimics voltage-gated K(+) channels, which provides a foundation for an improv

290 HO downregulates alveolar K(2P)2.1 (TREK-1) K(+) channels, which results in worsening lung injury.

291 body, which contains glomus cells expressing K(+) channels whose inhibition by hypoxia leads to trans

292 es binding to the transmembrane surface of a K(+) channel will result in displacement of a phospholip

293 on of physiologically relevant regulators of K(+) channels will aid in the design of approaches that

294 discovered to block human voltage-gated KCNQ K(+) channels with a 2.5 muM K(d).

295 echanisms controlling selective transport in K(+) channels with a nonconventional SF sequence.

296 nding sites ("hot spots") for cholesterol on K(+) channels with characteristics that match those of k

297 at is conserved across different families of K(+) channels with implications for rational drug design

298 ), inward rectifier Kir7.1, Ca(2+)-activated K(+) channels with large (KCNMA1, Slo1), small (KCNN1-3)

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

300 ly predicted the response of a voltage-gated K(+) channel within a phospholipid bilayer membrane to a