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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.
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
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
39 gene variant, supporting the hypothesis that K(+) channels affect the metabolic responses of fat cell
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(
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
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
55 tivity of large-conductance Ca(2+)-activated K(+) channels and the expression of MaxiKalpha was decre
57 solute uptake via physical interactions with K(+) channels and to moderate their gating at the plasma
60 physiological connections between the NALCN, K(+) channels, and gap junctions that mediate regulation
62 KEY POINTS: Repolarizing currents through K(+) channels are essential for proper sinoatrial node (
64 d small-conductance (KCa2) calcium-activated K(+) channels are gated by calcium binding to calmodulin
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
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
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,
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
86 5 Pf clones, low inhibitory activity in hERG K(+) channel blockage testing, negativity in the Ames te
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
94 the human ether-a-go-go-related gene (HERG) K(+) channel by inhibiting the corresponding current, IK
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
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
103 st experimental evidence that oxidation of a K(+) channel constitutes a mechanism of neuronal and cog
105 mediated by Ether-a-go-go-Related Gene (ERG) K(+) channels contributes to persistent firing in neocor
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
111 KCNE3 was the first reported skeletal muscle K(+) channel disease gene, but the requirement for KCNE3
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
118 imination of TASK-2 (K(2P)5), a pH-sensitive K(+) channel expressed in RTN neurons, essentially aboli
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
124 n K(+) channels (K2P) were identified as the K(+) channel family mediating BUNV K(+) channel dependen
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(
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
139 ree other members of the ether-a-go-go (EAG) K(+) channel gene family, including EAG1 (Kv10.1), ERG3
141 hanced activation of the G-protein-activated K(+) channel (GIRK; Kir3.1/Kir3.4) was shown when mutant
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
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(+
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
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 (
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
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
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
183 tidine phosphorylation and activation of the K(+) channel KCa3.1, which is required for TCR-stimulate
185 he intermediate-conductance Ca(2+)-activated K(+) channel (KCa3.1) constitutes an attractive pharmaco
188 SIGNIFICANCE STATEMENT Slack Na(+)-activated K(+) channels (KCNT1, KNa1.1) regulate neuronal excitabi
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
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
199 uctance KCa (BK) and other voltage-dependent K(+) channels (Kv) are highly expressed in carotid body
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
208 On the other hand, numerous ligand-gated K(+) channels lack such gate, suggesting that they may b
210 necessary signal for the modulation of Kv2.1 K(+) channel localization and physiological function.
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
217 he Kv4 complex, this study demonstrates that 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
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
230 because they form a channel complex with the K(+) channel pore-forming subunit Kv4.3 in a subset of n
233 endothelial cells lack the Ca(2+) -activated K(+) channels present in arterial endothelium to generat
239 betes, we found that activation of the TRESK K(+) channel reduced NG excitability and disrupted gastr
245 hods to determine how Kv3.4, a voltage-gated K(+) channel robustly expressed in dorsal root ganglion
247 exity of the conformational landscape of the K(+) channel selectivity filter and its dependence on th
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
254 BSTRACT: Small conductance Ca(2+) -activated K(+) channels (SK) play an important role in regulating
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
262 present study, we show that inward rectifier K(+) channel subfamily 2 isoform 1 (Kir2.1) currents non
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-
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
271 he expression of Twik-related acid-sensitive K(+) channel (TASK)-1 [a pH-sensitive potassium channel
273 b, and KCTD16 subunits (named after their T1 K(+)-channel tetramerization domain) that regulate G-pro
275 Therefore, we have identified a lysosomal K(+) channel that provides a positive feedback mechanism
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
287 and Twik-related arachidonic-acid stimulated K(+) channel (TRAAK) form the TREK subfamily of two-pore
291 to drive membrane fusion, binds to the KAT1 K(+) channel via two sites on the protein, only one of w
295 the HERG (human ether-a-go-go-related gene) K(+) channel, which conducts the rapidly activating dela
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 (
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