ライフサイエンスコーパス: SK channel

1 e-related modulation of the apamin-sensitive SK channel.

2 rate set by the deactivation kinetics of the SK channel.

3 (+) cells that were inhibited by blockers of SK channels.

4 Rac1 in synaptic compartments and modulating SK channels.

5 2+) sensing by CaM and mechanical opening of SK channels.

6 pharmacological targets of riluzole include SK channels.

7 ensory neurons possibly via Ca(2+)-activated SK channels.

8 hrough the endoplasmic reticulum to activate SK channels.

9 detect binding events between the apamin and SK channels.

10 artially due to blockade of apamin-sensitive SK channels.

11 ligand to study the activation properties of SK channels.

12 a selective antagonist of calcium-activated SK channels.

13 es of the interaction between calmodulin and SK channels.

14 elevates intracellular Ca(2+) and activates SK channels.

15 rminus kinase, or P38 alone had no effect on SK channels.

16 sequential activation of alpha9/alpha10 and SK channels.

17 otropic neurotransmitter receptors, activate SK channels.

18 in the trafficking and/or function of IK and SK channels.

19 actions were also inhibited by activation of SK channels.

20 on conductance that coupled to activation of SK channels.

21 ed by Ca(2+) -dependent activation of IK and SK channels.

22 re unaffected by inhibitors of TRPV4, IK and SK channels.

23 and a decrease in the functional activity of SK channels.

24 did not affect currents through TRPV4, IK or SK channels.

25 of Ca(2+)-activated small-conductance K(+) (SK) channels.

26 he small conductance, Ca(2+)-activated K(+) (SK) channels.

27 and small conductance Ca(2+)-activated K(+) (SK) channels.

28 g those associated with 'small-conductance' (SK) channels.

29 by small-conductance Ca(2+)-activated K(+) (SK) channels.

30 m small conductance calcium-gated potassium (SK) channels.

31 sed small conductance Ca(2+)-activated K(+) (SK) channels.

32 all-conductance calcium-activated potassium (SK) channels.

33 vity of small conductance Ca2+-activated K+ (SK) channels.

34 rather than a specific molecular coupling to SK channels accounts for the reduced SFA of Ca(v)1.3(-/-

35 we also find that KCNQ and apamin-sensitive SK channels act synergistically to regulate firing rate

36 In contrast, SK channels activated by APs at the soma of these neuron

37 Additionally, SK channels activated by Tb(3+) demonstrate a remarkably

38 ice, we investigated the role of Ca(v)1.3 on SK channel activation and how this functional coupling a

39 n response to increases in EC calcium and IK/SK channel activation and suggest that EC Kir channels c

40 examined purinergic receptor (P2Y) mediated SK channel activation as a mechanism for purinergic rela

41 action potentials (APs), and compare this to SK channel activation at the soma.

42 As a result SK channel activation by backpropagating APs gated STDP

43 This A(1)-mediated, prolonged SK channel activation has not been described previously.

44 hen K(V)7/M channel activity is compromised, SK channel activation significantly and uniquely reduces

45 pe) Ca(2+) channels as the Ca(2+) source for SK channel activation.

46 determines the kinetics and consequences of SK channel activation.

47 SK-channel activation and the subsequent reduction in Ca

48 p4A is a potent native agonist for P2Y1R and SK-channel activation in human and mouse colon.

49 An SK channel activator (SKA-31) decreased contractions dur

50 agment, itself a target for drugs modulating SK channel activities, plays a unique role in coupling C

51 ortantly, we demonstrate that Rac1 modulates SK channel activity and firing patterns of Purkinje cell

52 The mechanism by which p75 regulates SK channel activity appears to involve its ability to ac

53 The consequences of SK channel activity have been revealed by the specific b

54 Ca) channels and identify distinct roles for SK channel activity in regulating calcium- versus sodium

55 To determine if SK channel activity was indeed eliminated, seconds-long

56 to investigate the effects of an enhancer of SK channel activity, 1-ethyl-benzimidazolinone (EBIO).

57 usive and SNX increases EPSPs independent of SK channel activity.

58 esicle release, and upregulated postsynaptic SK channel activity.

59 ponses in CA1 neurons by decreasing synaptic SK channel activity.

60 e rescued by pharmacological augmentation of SK channel activity.

61 mall conductance Ca(2+)-activated potassium (SK) channel activity in Purkinje cells from p75(-/-) mic

62 ceptor potential vanilloid 4) channel and IK/SK channel agonists were highly attenuated by Kir channe

63 SK channels allow efflux of potassium ions when intracel

64 nism where M(1) receptor activation inhibits SK channels, allowing enhanced NMDAR activity and leadin

65 es that link Ca(2+) influx through NMDARs to SK channels and Ca(2+) influx through R-type Ca(2+) chan

66 vated K(+) channels (i.e., small-conductance SK channels and large-conductance BK channels).

67 enous SK currents, reducing coupling between SK channels and NMDA receptors (NMDARs) and increasing p

68 improves motor neuron function by acting on SK channels and suggest that SK channels may be importan

69 s the molecular and functional properties of SK channels and their physiological roles in central neu

70 omolecular complex in which the Ca2+ source, SK channels and various modulators are assembled determi

71 all-conductance calcium-activated potassium (SK) channel and CB1 cannabinoid receptor activation.

72 umen via both ROMK-like small-conductance K (SK) channels and Ca2+ -activated big-conductance K (BK)

73 of small-conductance Ca(2+)-activated K(+) (SK) channels and reveals an important role for both SK2

74 Small conductance Ca(2+)-activated K(+) (SK) channels and voltage-gated A-type Kv4 channels shape

75 c signal integration, via over-activation of SK channels, and synapse plasticity, phenotypes rescued

76 cium-dependent small conductance potassium ('SK') channels, and longer-lasting and voltage-dependent

77 cium-dependent small conductance potassium ('SK') channels, and longer-lasting and voltage-dependent

78 s, small conductance Ca-activated potassium (SK) channels, and NMDA receptors.

79 Injections of the specific SK channel antagonist apamin into PLC increased Fos expr

80 SK channels are a potential pharmacological target for m

81 In CA1 dendrites, SK channels are activated by Ca2+ through NMDA receptors

82 ing somatic excitability in central neurons, SK channels are also expressed in the postsynaptic membr

83 aximum firing rate of Purkinje neurons; when SK channels are blocked by the specific antagonists apam

84 SK channels are Ca2+-activated K+ channels that underlie

85 ore, we also show that KCNQ channels but not SK channels are downstream effectors of serotonin modula

86 lockers, we provide evidence that functional SK channels are expressed in the somata and proximal den

87 SK channels are likely encoded by three genes, Kcnn1-3,

88 We find that in mice, SK channels are localized to dendritic spines, and their

89 e receptors are Ca(2+)-impermeable, and thus SK channels are not efficiently activated by synaptic ac

90 ced the same result, suggesting that somatic SK channels are not tightly colocalized with their calci

91 Because SK channels are predominantly expressed in atrial myocyt

92 SK channels are predominantly expressed in the atria as

93 SK channels are proposed to be assembled as tetramers si

94 ith this, mRNA levels for the SK3 subunit of SK channels are significantly higher in ventral CA1 pyra

95 SK channels are stable macromolecular complexes of the i

96 SK channels are tightly coupled to synaptically activate

97 We found that SK channels are tonically activated and contribute to th

98 Interestingly, SK channels are transiently activated by calcium sparks

99 These results provide further evidence that SK channels are unlikely to underlie the sAHP.

100 all conductance calcium-activated potassium (SK) channels are required for the slow inhibitory compon

101 mall conductance Ca2+-activated K+ channels (SK channels) are heteromeric complexes of pore-forming a

102 ctance calcium-activated potassium channels (SK channels) are present in spines and can be activated

103 ated voltage-independent potassium channels (SK channels) are widely expressed in diverse tissues; ho

104 -conductance Ca(2+)-activated K(+) channels (SK channels) are widely expressed throughout the central

105 We propose SK channels as a potential target for modulating SAN rat

106 compound an ideal tool to assess the role of SK channels as possible targets for the treatment of dis

107 ramidal cell excitability and highlights BLA SK channels as promising targets for the treatment of an

108 While SK channels at the soma have long been known to contribu

109 that the conformation of the ID fragment in SK channels becomes readily identifiable in the presence

110 ical and pharmacological hallmarks of native SK channels, being gated solely by intracellular Ca(2+)

111 t under control conditions but present after SK channel block.

112 SK channel blockade abolished the mAHP and revealed an a

113 SK channel blockade caused a small depolarization in spi

114 bath application of apamin, suggesting that SK channel blockade likely increased excitability by a p

115 urons increased twice as much in response to SK channel blockade relative to EPSPs recorded from WT C

116 SK channel blockade slows repolarization and subsequent

117 SK channel blockade with apamin or UCL1684 increased the

118 hreshold depolarization was increased during SK channel blockade, indicating that depolarizing input

119 ne + 10 microM CGP55845) was occluded by the SK channel blocker apamin (300 nM-1 microM) which in its

120 c plasticity is mimicked and occluded by the SK channel blocker apamin and is absent in Purkinje cell

121 nhibitory current by 56 +/- 12%, whereas the SK channel blocker apamin decreased the NECA-induced cur

122 Moreover, the SK channel blocker apamin enhanced the input-output func

123 Moreover, UCL2077 and apamin, a selective SK channel blocker, affected spike firing in hippocampal

124 d by Ca(2+)-activated slow conductance K(+) (SK) channel blocker apamin.

125 Local application of bicuculline but not the SK-channel blocker apamin attenuated the effects of LHb

126 TRPV4 and SK channel blockers also increased contractions of intac

127 These results suggest SK channel blockers as potentially interesting anti-AF d

128 applications of irreversible and reversible SK channel blockers, we provide evidence that functional

129 ntiation by DCEBIO and NS309 was reversed by SK channel blockers.

130 r study reveals a new level of regulation of SK channels by cAMP-PKA and suggests that ion channel to

131 Furthermore, LTP requires inhibition of SK channels by mGluR1, which removes a negative feedback

132 ion of P38 and ERK and that MAPK inhibit the SK channels by stimulating PTK expression and via a PTK-

133 We found that SK channels can be fully activated by nanomolar concentr

134 hese findings suggest that Ca(2+) -sensitive SK channels can translate changes in cellular Ca(2+) int

135 chemical studies suggests that in the intact SK channel complex, the N-lobe of calmodulin provides li

136 hat small-conductance Ca(2+)-activated K(+) (SK) channels constitute a new target for treatment of at

137 T-type calcium, BK, and SK channels contributed to interspike and interburst int

138 ot changes in Ca(2+) -mediated activation of SK channels, contributes to exacerbated MNC activity in

139 The SK channel contribution to excitatory postsynaptic poten

140 However, the precise mechanisms by which SK-channels control the induction of synaptic plasticity

141 ated whether the Ca(2+) -sensitive nature of SK channels could explain arrhythmic SAN pacemaker activ

142 Inhibition of SK channels decreased AP firing frequency by 66% and inc

143 Potassium currents through SK channels demonstrate inward rectification, which furt

144 We also show that SK channel dendritic distribution is dynamic and under t

145 Blocking SK channels disrupted the one-to-one signal transmission

146 mplementary approaches, we found that native SK channel distribution in pyramidal neurons, across the

147 (V)7/M channels are operative, activation of SK channels during repetitive firing does not notably af

148 that postsynaptic activation of K(V)1.x and SK channels during spiking suppresses the subsequent eff

149 uture studies will examine the expression of SK channels during the aging process in GnRH neurons.

150 eal a causal link for the first time between SK channel dysregulation and 5-HT neuron activity in a l

151 We find that somatic SK channels effectively limit the maximum firing rate of

152 he effects of the recently identified potent SK channel enhancer NS309 on recombinant SK2 channels, n

153 has recently benefited from the discovery of SK channel enhancers, the prototype of which is 1-EBIO.

154 ein kinase A (PKA) levels, strongly limiting SK channel expression at the pyramidal neuron soma.

155 Our studies suggest that a reduction in SK channel expression, but not changes in Ca(2+) -mediat

156 Thus, blocking SK channels facilitates the induction of long-term poten

157 The expression of all three members of the SK channel family was quantified by PCR.

158 y suggest that the calcium is present at the SK channel for a very short time after each action poten

159 We find that native SK channels from rat hippocampal neurons reside primaril

160 Although an increased SK channel function contributes to adaptive physiologica

161 The elucidation of SK channel function has recently benefited from the disc

162 t that a posttranslational downregulation of SK channel function in thin distal dendrites is a signif

163 GluN3A knock-out mice, cocaine did not alter SK channel function or VTA DA neuron firing.

164 scular defects in a C. elegans SMA model and SK channel function was required for this beneficial eff

165 eveal that chronic adolescent stress impairs SK channel function, which contributes to an increase in

166 onses, it remains unknown whether changes in SK channel function/expression contribute to exacerbated

167 ansgenic mice, each lacking one of the three SK channel genes expressed in the CNS, reveals that mice

168 We conclude that SK channels have demonstrable effects on SAN pacemaking

169 ABSTRACT: Small conductance K(+) (SK) channels have been implicated as modulators of spont

170 conductance Ca(2+)-activated K(+) channels (SK channels) have been reported in excitable cells, wher

171 he present studies was to define the role of SK channels in Ca 2+ -dependent cholangiocyte secretion.

172 In CA1 pyramidal cells, SK channels in dendritic spines were shown to regulate s

173 t studies have revealed unexpected roles for SK channels in fine-tuning intrinsic cell firing propert

174 ere we report that CaCCs coexist with BK and SK channels in inferior olivary (IO) neurons that send c

175 strategy may help define the in vivo role of SK channels in other neuronal pathways.

176 ) influx through TRPV4 channels can activate SK channels in PDGFRalpha(+) cells and prevent bladder o

177 We conclude that SK channels in spines and dendrites of cortical pyramida

178 Here we investigate the activation of SK channels in spines and dendrites of rat cortical pyra

179 These findings indicate that activation of SK channels in spines by backpropagating APs plays a key

180 etermining the intrinsic open probability of SK channels in the absence of Ca(2+), affecting the appa

181 s differential expression with more abundant SK channels in the atria and pacemaking tissues compared

182 tudy the effect of inhibiting P38 and ERK on SK channels in the cortical collecting duct from rats th

183 yonic development suggests an involvement of SK channels in the regulation of developmental processes

184 However, the presence of functional SK channels in the somata and their role in controlling

185 all-conductance calcium-activated potassium (SK) channels in rat MNTB principal neurons.

186 all-conductance calcium-activated potassium (SK) channels in the MNTB neurons from rats of either sex

187 of Ca(2+) -activated small conductance K(+) (SK) channels in the murine SAN.

188 of small conductance Ca(2+)-activated K(+) (SK) channels in these cells is far higher ( approximatel

189 Activation of SK channels increased mitochondrial K(+) currents, where

190 Blocking SK channels increased the amount of long-term potentiati

191 l inhibition of calcium-activated potassium (SK) channels increases the variability in their firing p

192 fication is in fact an intrinsic property of SK channels independent of intracellular blockers.

193 -conductance Ca(2+)-activated K(+) channels (SK channels) influence the induction of synaptic plastic

194 Blockers of TRPV4 or SK channels inhibited currents activated by GSK and incr

195 When the SK channel inhibitor AP14145 was tested in these animals

196 gesting that in physiological conditions the SK channel is significantly activated by Ca(2+) influx t

197 pecific subcellular membrane localization of SK channels is likely to represent the basis for a choli

198 ive small-conductance Ca(2+)-activated K(+) (SK) channels is responsible for the postshock APD shorte

199 le and subcellular localization of different SK channel isoforms in lumbar spinal alpha-motoneurons (

200 Studies of SK channel knock-out mice reveal that of the three apami

201 We imaged SK channels labeled with fluorophore-tagged apamin and m

202 ity produces intermittent hyperactivation of SK channels, leading to arrhythmic pauses alternating wi

203 ration action potentials secondarily recruit SK channels, leading to greater spike frequency adaptati

204 on by acting on SK channels and suggest that SK channels may be important therapeutic targets for SMA

205 all-conductance calcium-activated potassium (SK) channels mediate a potassium conductance in the brai

206 all-conductance calcium-activated potassium (SK) channels mediate medium after-hyperpolarization (AHP

207 ed a common cellular mechanism (reduction in SK channel-mediated AHP) that led to the learning-induce

208 ponse composed of a transient Ca2+-dependent SK channel-mediated hyperpolarization and a TRPC-mediate

209 The generation and magnitude of the SK channel-mediated hyperpolarization depended solely on

210 primary resonance was also influenced by the SK channel-mediated medium AHP (mAHP), because the SK bl

211 utput function, and also that a reduction in SK channel-mediated, apamin-sensitive AHP is a critical

212 Up4A induced P2Y1R-SK-channel-mediated hyperpolarization in isolated PDGFRa

213 lcium-activated small conductance potassium (SK) channel member SK3 and mitochondrial ROS.

214 -conductance Ca(2+)-activated K(+) channels (SK channels) modulate excitability and curtail excitator

215 all-conductance, Ca2+-activated K+ channels (SK channels) modulate neuronal excitability in CA1 neuro

216 Bath application of a positive SK channel modulator (1-EBIO) normalized firing in ex vi

217 That EBIO is an SK channel modulator was confirmed by its potentiation o

218 SK channel modulators, CyPPA and SKA-31, induced signifi

219 with fluorophore-tagged apamin and monitored SK channel nanoclustering at the single molecule level b

220 d residues in the S6 transmembrane domain of SK channels near the inner mouth of the pore that collec

221 In vivo, we demonstrate that inhibiting SK channels normalizes chronic social isolation-induced

222 High K intake increased SK channel number per patch and increased the ROMK chann

223 gene is solely responsible for encoding the SK channels of inner hair cells.

224 Further, we found that the impact of SK channels on the SMT critically depended on the voltag

225 of the small-conductance Ca2+ -dependent K+ (SK) channels, or their interaction with Ca2+, underlies

226 SK channels play a role in setting the intrinsic firing

227 r of spikes fired in bursts, indicating that SK channels play an important role in maintaining dopami

228 These data reveal that SK channels play crucial roles in regulating the resting

229 We conclude that although SK channels play little role in generating SFA in PVN-RV

230 all-conductance calcium-activated potassium (SK) channels play an important role in regulating neuron

231 S: Small conductance Ca(2+) -activated K(+) (SK) channels play an important role in regulating the ex

232 Small-conductance Ca(2+)-activated K(+) (SK) channels play essential roles in the regulation of c

233 reduced expression of small-conductance Kca (SK) channel protein in the BLA of socially isolated (SI)

234 Therefore, proximal SK channels provide a "second line of defense" against i

235 We speculate that SK channels provide a mechanism for rapidly sensing chan

236 Heterologously expressed SK channels recapitulate the biophysical and pharmacolog

237 aspartate receptors (NMDARs) activates spine SK channels, reducing EPSPs and the associated spine hea

238 e calcium-dependent potassium (SK) channels; SK channels regulate firing of VTA DA neurons, but this

239 on laser uncaging of glutamate, we show that SK channels regulate NMDAR-dependent Ca(2+) influx withi

240 all-conductance calcium-activated potassium (SK) channels regulate action potential firing and shape

241 lly-plausible, dendritic spine, we show that SK-channels regulate calmodulin activation specifically

242 indicate that a dorsal-ventral difference in SK channel regulation of NMDAR activation has a profound

243 all-conductance calcium-activated potassium (SK) channels, regulators of firing frequency, were silen

244 The coactivation of GIRK and SK channels represents a novel mechanism of adenosine-me

245 ur model further predicts that inhibition of SK channels results in a depolarisation of action potent

246 through CaV(2.3) VSCCs selectively activates SK channels, revealing the presence of functional Ca mic

247 Small conductance Ca(2+)-activated K(+) (SK) channels sense intracellular Ca(2+) concentrations v

248 SK channels show a distinct subcellular localization tha

249 all-conductance calcium-dependent potassium (SK) channels; SK channels regulate firing of VTA DA neur

250 Blocking all SK channel subtypes with apamin facilitates the inductio

251 also identified specific roles for different SK channel subtypes.

252 ns lead to the adult expression map for each SK channel subunit and how their coexpression in the sam

253 Three isoforms of SK channel subunits (SK1, SK2, and SK3) are found to be

254 ce reveal that of the three apamin-sensitive SK channel subunits (SK1-SK3), only SK2 subunits are nec

255 The three SK channel subunits display different developmental expr

256 f heteromultimeric complexes among different SK channel subunits in atrial myocytes.

257 f heteromultimeric complexes among different SK channel subunits in native cardiac tissues.

258 e onset of expression and regions expressing SK channel subunits in the embryonic and postnatal devel

259 pecific ligands of the different isoforms of SK channel subunits may offer a unique therapeutic oppor

260 Real-time PCR measurements of SK channel subunits mRNA in supraoptic nucleus punches r

261 e is known about the molecular regulation of SK channel subunits.

262 the past two decades, positive modulators of SK channels such as NS309 and 1-EBIO have been developed

263 gCRND8 cortex by pharmacological blockade of SK channels, suggesting a novel target for the treatment

264 els supporting faster synaptic waveforms and SK channels supporting slower synaptic waveforms.

265 HP) and increased spontaneous firing through SK channel suppression, indicative of DCN hyperexcitabil

266 Ca(v)1.3 slows down MCC firing by activating SK channels that maintain Na(V) channel availability hig

267 nd to enhance NMDAR activation by inhibiting SK channels that otherwise act to hyperpolarize postsyna

268 naptic potential (EPSP), Ca(2+) influx opens SK channels that provide a local shunting current to red

269 is associated with an enhanced activation of SK channels that strongly suppresses NMDAR activation at

270 ward currents and produce a model for BK and SK channels that we use to reproduce the outward current

271 of small conductance Ca-activated potassium (SK) channels that are found in the spine, resulting in i

272 m-sensitive calcium conductance coupled with SK channels, that is pharmacologically distinct from L-,

273 luding the small conductance activated K(+) (SK) channels, that maybe modulated by this signaling pat

274 2+)-activated K(+) channels, known as BK and SK channels, the physiological importance of Ca(2+)-acti

275 regulation of ROMK-like small-conductance K (SK) channels, the patch-clamp technique was used to stud

276 iate and small conductance potassium (IK and SK) channels, thereby causing hyperpolarization and endo

277 SK channels thus underlie repolarization of dendritic pl

278 ng and the high Ca(2+) sensitivity of IK and SK channels to cause vasodilation.

279 To allow studies on the contribution of SK channels to different phases of development of single

280 RPV4 sparklet-mediated stimulation of IK and SK channels to promote vasodilation.

281 g apamin, a toxin that specifically binds to SK channels, to the tip of an AFM cantilever, we are abl

282 Understanding the mechanisms of SK channel trafficking may provide new insights into the

283 SK channel transcripts are expressed at early stages of

284 SK channels underlie important physiological functions b

285 are necessary for the ImAHP, and none of the SK channels underlie the IsAHP.

286 The effect of inhibiting MAPK on SK channels was not affected in the presence of herbimyc

287 l conductance Ca(2)(+) -activated potassium (SK) channel was developed and incorporated into a physio

288 ated by small-conductance Ca2+-dependent K+ (SK) channels was critical for the precision of autonomou

289 Moreover, SK channels were activated by action potentials and affe

290 SK channels were activated by intracellular Ca(2+) spark

291 SK channels were activated, in part, by Ca(2+) flowing t

292 SK channels were also activated by Ca(2+) influx through

293 onic cAMP-PKA levels also controlled whether SK channels were expressed in nanodomains as single enti

294 f muscarinic receptors, TRPV4 channels or IK/SK channels were reduced, but not eliminated, by Kir cha

295 s during autonomous firing were reduced when SK channels were removed, and a nearly equal reduction i

296 The presence and functional activity of SK channels were therefore investigated in the human len

297 ly regulated by Ca2+ -activated K+ channels (SK-channels) which are in turn inhibited by neuromodulat

298 Blocking SK channels with apamin depolarized the resting membrane

299 aging, we demonstrate that the inhibition of SK channels with apamin results in a location-dependent

300 Inhibition of SK channels with the specific blocker apamin prolonged a