ライフサイエンスコーパス: SK

1 SK blockade partially suppressed the arrhythmic burst pa

2 SK channel blockade slows repolarization and subsequent

3 SK channels are a potential pharmacological target for m

4 SK channels are predominantly expressed in the atria as

5 SK channels are voltage independent and their gating is

6 SK channels in the NAcS may serve as a target to treat a

7 SK channels show a distinct subcellular localization tha

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

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

10 SK currents play a role in porcine atrial repolarization

11 SK NEP1 was tested as well.

12 SK phosphorylates sphingosine producing the potent signa

13 SK-N-SH neuronal cells were exposed to active recombinan

14 itro IC50 values were 11-48 ng/mL in HER2 3+ SK-BR-3 and KPL-4 (7 inactive) for the anti-HER2 ADCs (H

15 s) of colonic muscle through activation of a SK conductance.

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

17 hrough the endoplasmic reticulum to activate SK channels.

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

19 ation leads to calcium influx that activates SK/IK channels and eNOS serine 1176 phosphorylation in E

20 o find that two specimens from South Africa, SK 96 (usually attributed to Paranthropus) and Stw 80 (H

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

22 of reversible competitive inhibitors against SK from Mycobacterium tuberculosis and Helicobacter pylo

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

24 urons were suppressed by preceding APs in an SK-dependent manner.

25 and the rectification characteristics of an SK channel determine its impact on early, plateau, and r

26 duce human melanoma cell lines SK-MEL-05 and SK-MEL-147 (both wild type p53).

27 Cs in co-culture with MCF-7, MDA-MB-231, and SK-BR-3 breast cancer cell lines using [Formula: see tex

28 Upon mensacarcin exposure, SK-Mel-28 and SK-Mel-5 melanoma cells, which have the BRAF(V600E) muta

29 sts resulted in upregulation of SPTLC1-3 and SK 1/2 expression.

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

31 2+)-activated K(+) channels, known as BK and SK channels, the physiological importance of Ca(2+)-acti

32 Pharmacological blockade of HCN and SK activities mimicked changes in firing, confirming tha

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

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

35 rmediate- and small-conductance K(+) (IK and SK) channels and endothelial nitric oxide synthase (eNOS

36 rmediate- and small-conductance K(+) (IK and SK) channels in some vascular beds and endothelial nitri

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

38 ermediate and small conductance K(+) (IK and SK, respectively) channels.

39 elanoma cells, specifically the LOX IMVI and SK-MEL-28 cell lines.

40 In NLF (biallelic NF1 inactivation) and SK-N-AS (NRAS Q61K) cell lines, trametinib caused a near

41 n, but persisted in the presence of KATP and SK antagonists.

42 d in MYCN amplified NB cell lines (Kelly and SK-N-BE(2)C) by Western blot (WB) and immunohistochemist

43 anoma cell lines (A375, Hs294t, SK-Mel28 and SK-Mel119) with cryptolepine (1.0, 2.5, 5.0 and 7.5 muM)

44 ng haplotype maps derived from B73, Mo17 and SK, we identified 80,614 polymorphic structural variants

45 studies demonstrate that in MNNs, NMDARs and SK channels are functionally coupled, forming a local ne

46 We report that NMDARs and SK channels form a functional Ca(2+) -dependent negative

47 However, whether NMDARs and SK channels in MNNs are functionally coupled, and whethe

48 his work, we investigated whether NMDARs and SK channels in MNNs are functionally coupled, and whethe

49 he negative feedback loop between NMDARs and SK channels was blunted or absent in MNNs of heart failu

50 sma membrane returns differentiated PC12 and SK-N-SH cells to an undifferentiated state.

51 in two neuroblastoma cell lines, SH-SY5Y and SK-N-BE(2).

52 TRPV4 and SK channel blockers also increased contractions of intac

53 This anomalous SK behavior enables simultaneous tuning of both TSQD siz

54 olarized PDGFRalpha(+) cells (the alpha1A AR-SK channel signal pathway).

55 g motor complexes (CMMCs) via the alpha1A AR-SK channel signal pathway.

56 mages and classified each dermoscopically as SK or not SK.

57 subcellular compartments of some neurons as SK channel subunits.

58 n 3 human neuroblastoma cell lines (SK-N-AS, SK-N-BE2, and SH-SY5Y), soluble HBEGF is sufficient to p

59 ment of the patient with chlorzoxazone, a BK/SK channel activator, partially improved motor function,

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

61 Blocking SK channels with apamin depolarized the resting membrane

62 sients activates, but higher [Ca(2+)] blocks SK channels, yielding a transient outward-like I(SK) tra

63 In both SK-N-AS and BE(2)C cell lines, when engrafted on the cho

64 midal cells and is recruited later than both SK and M currents.

65 ent of dopamine normalized HCN activity, but SK current remained depressed.

66 m afterhyperpolarization (mAHP), mediated by SK channels, and SK3 protein levels in the NAcS decrease

67 litude of mAHP of NAcS MSNs were reversed by SK channel activator 1-EBIO and mimicked by the SK chann

68 y leads to LL HC hyperpolarization served by SK channels.SIGNIFICANCE STATEMENT The fish lateral line

69 No such departure from the canonical SK growth regime has been reported previously.

70 Human melanoma cells (SK-MEL-28) transfected with APCN cDNA acquired the abili

71 uctance calcium-activated potassium channel (SK) subunits have been cloned and found to preferentiall

72 conductance Ca(2+) -activated K(+) channels (SK) play an important role in regulating the activity of

73 onductance, Ca(2+) -activated K(+) channels (SK, KCa 2) are expressed in human atrial myocytes and ar

74 onductance, Ca(2+) -activated K(+) channels (SK, KCa 2) are unique subclasses of K(+) channels that a

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

76 ctance calcium-activated potassium channels (SK channels) on dendritic excitability in male and femal

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

78 We report that fidelity of cholinergic SK responses requires the continued presence of extracel

79 munostaining to determine small conductance (SK) calcium-activated potassium channel protein levels.

80 ese data indicate that somatic and dendritic SK channels have opposite effects on neuronal excitabili

81 n to the cortical surface to block dendritic SK channels shifted the distribution of action potential

82 potential output, whereas blocking dendritic SK channels paradoxically reduces the generation of dend

83 The effect of apamin on dendritic SK channels was occluded when R-type calcium channels we

84 cts on neuronal excitability, with dendritic SK channels counter-intuitively promoting rather than su

85 t on the downregulation of calcium-dependent SK-type K(+) channels, which contribute to a medium-slow

86 independent risk markers of dermoscopically SK-like melanomas.

87 st score of 4.4 (2.3), while dermoscopically SK-like melanomas achieved a total dermoscopy score of o

88 patterns of (clinically and dermoscopically) SK-like melanomas, patient demographics, and interobserv

89 ost helpful criteria in correctly diagnosing SK-like melanomas were the presence of blue-white veil,

90 To illustrate the utility of the diverse SK line, we used it to perform map-based cloning of a ma

91 dult anxiety-like behavior by downregulating SK channel function and protein expression, which leads

92 Moreover, enhanced SK activity contributes to the adaptive responses of MNC

93 ndings show that SKIP re-expression enhances SK activity in leukemia cells.

94 Upon mensacarcin exposure, SK-Mel-28 and SK-Mel-5 melanoma cells, which have the BR

95 stamine with reduced extravasation of fluid, SK-1 activity, proinflammatory cytokine and chemokine pr

96 For SK-MEL-05, tumor inhibition was similar in nude and Nod-

97 complete inhibition of tumor progression for SK-MEL-147 when using nude mice with no evidence of hepa

98 id mice and was less efficient than seen for SK-MEL-147, indicating both cell type and host specific

99 and CWM decreased as follows: PC > FL > ST > SK.

100 ivity on a number of tumor cell lines (HeLa, SK-MEL-28, A549, MCF-7) with effective concentrations (E

101 ls isolated from the NCX KO exhibited higher SK current than wildtype (WT) and apamin prolonged their

102 of human melanoma cell lines (A375, Hs294t, SK-Mel28 and SK-Mel119) with cryptolepine (1.0, 2.5, 5.0

103 PKA phosphorylation attenuates I(SK) rectification by reducing the Ca(2+) /voltage-depend

104 a(2+)-dependent block is released, causing I(SK) to rise again and contribute to repolarization.

105 ated solely by Ca(2+), but the SK current (I(SK)) is inwardly rectified.

106 on (isoproterenol, 100 nmol L(-1) ) evoked I(SK) in VMs from Shams, resulting in shortening of action

107 activating at low [Ca(2+)] yet inhibiting I(SK) at high [Ca(2+)].

108 hannels, yielding a transient outward-like I(SK) trajectory.

109 howing that intrinsic rectification limits I(SK) at high V(m) during the early and plateau phase of A

110 The typical profile of I(SK) during AP clamp included an initial peak (mean 1.6 p

111 K channel model replicates key features of I(SK) recording during AP clamp showing that intrinsic rec

112 We examined the effect of I(SK) rectification on APs in rat cardiomyocytes by simult

113 A phosphorylation lessens rectification of I(SK) via reduction Ca(2+) /voltage-dependent inhibition o

114 Thus, Ca(2+) has a biphasic effect on I(SK), activating at low [Ca(2+)] yet inhibiting I(SK) at

115 Mg(2+)-dependent rectification to simulate I(SK) and investigated the relative contributions of each

116 During the rest of the AP stimulus, I(SK) either plateaued or gradually increased as the cell

117 Therefore, I(SK) is an important repolarizing current, and the rectif

118 IK/SK channels co-localized with TRPV4(EC) channels at myoe

119 GSK1016790A (10 nm) selectively activated IK/SK channels in MAs and eNOS in PAs, revealing preferenti

120 in PAs, revealing preferential TRPV4(EC) -IK/SK channel coupling in MAs and TRPV4(EC) -eNOS coupling

121 ry arteries, which may explain TRPV4(EC) -IK/SK channel coupling in mesenteric arteries and its absen

122 signalling elements determines TRPV4(EC) -IK/SK vs. TRPV4(EC) -eNOS coupling in resistance arteries.

123 rototypes for arteries with predominantly IK/SK channel- and eNOS-dependent vasodilatation, respectiv

124 (EC) sparklets preferentially couple with IK/SK channels in mesenteric arteries and with eNOS in pulm

125 TRPV4(EC) channels co-localize with IK/SK channels in mesenteric arteries but not in pulmonary

126 rifosine on proteome and lysine acetylome in SK-N-AS cells and expands our understanding of the mecha

127 ellular senescence and migration activity in SK-N-SH cells.

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

129 Nevertheless, whether changes in SK function/expression contribute to exacerbated MNC act

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

131 ctivation of GM2-synthase mRNA expression in SK-RC-45 cells was accompanied by Sp1 and HDAC1 loss fro

132 or senescence, were significantly induced in SK-N-SH cells subjected to either PRMT1-KD or inhibitor

133 lysine acetylation sites were quantified in SK-N-AS cells and 216 differentially expressed proteins

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

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

136 -out dramatically decreased 5-HT staining in SK-N-SH cells as well as 5-HT concentrations in the cult

137 and acetylome after perifosine treatment in SK-N-AS neuroblastoma cells using SILAC labeling, affini

138 M3 formation took >= 7 years in SK 835 and completion of the roots would have occurred b

139 Although an increased SK channel function contributes to adaptive physiologica

140 cted leukemia cell lines exhibited increased SK activity.

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

142 gest that dysfunction of voltage-independent SK channels is the primary cause of CA3 neuronal hyperex

143 pens up a new avenue in treating HSV-induced SK lesions by increasing the stability and function of r

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

145 re-operated calcium entry channel inhibitor (SK&F96365) also reduced MSU crystal-induced NET release.

146 fying hypothesis' that rundown of inhibitory SK responses at resting membrane potentials (RMPs) refle

147 allenge the notion that SKIP always inhibits SK activity.

148 evious results indicating that SKIP inhibits SK function in fibroblasts and therefore challenge the n

149 Interestingly, SK channels are transiently activated by calcium sparks

150 soma, was dendritic in origin, and involved SK-dependent suppression of NMDA receptor activation.

151 ess small conductance Ca(2+)-activated K(+) (SK) and TRPV4 channels.

152 iac small conductance Ca(2+)-activated K(+) (SK) channels are activated solely by Ca(2+), but the SK

153 nd small conductance Ca(2+) -activated K(+) (SK) channels are critical synaptic and intrinsic mechani

154 nd small conductance Ca(2+) -activated K(+) (SK) channels are critical synaptic and intrinsic mechani

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

156 of small-conductance Ca(2+)-activated K(+) (SK) channels did not produce similar effects.

157 Small-conductance Ca(2+) -activated K(+) (SK) channels expressed in ventricular myocytes (VMs) are

158 Small-conductance Ca(2+) -activated K(+) (SK) channels expressed in ventricular myocytes are dorma

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

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

161 the small-conductance Ca(2+)-activated K(+) (SK) channels that are part of a multiprotein complex con

162 a small conductance Ca(2+) -activated K(+) (SK) conductance, evoked outward currents and hyperpolari

163 conductance calcium (Ca(2+))-activated K(+) (SK) currents in both male and female mice, leading to de

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

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

166 he DNA damage and ROS levels of the PRMT1-KD SK-N-SH cells were slightly increased.

167 can be effective to limit stromal keratitis (SK) lesion severity.

168 Seborrheic keratoses (SKs) are common benign skin tumors that share many morph

169 that clinically mimic seborrheic keratosis (SK) can delay diagnosis and adequate treatment.

170 nent systems (TCSs), having a sensor kinase (SK) and a cognate response regulator (RR), enable the hu

171 le pathways comprise a single sensor kinase (SK) that detects a signal and activates a response regul

172 inding (SB) domains of the shikimate kinase (SK) enzyme have been exploited in the development of rev

173 transferase subunits and sphingosine kinase (SK) 1/2 mRNA.

174 protein (SKIP) inhibits sphingosine kinase (SK) function in fibroblasts.

175 The sphingosine kinase (SK) pathway is an important regulator of vascular beds,

176 nflammation involves the sphingosine kinase (SK)/sphingosine-1-phosphate axis.

177 Oct4, along with Sox2 and Klf4 (SK), can induce pluripotency but structurally similar fa

178 assembly for the K. marmoratus South Korea (SK) strain highlighting the diversity and distribution o

179 ates from the well-known Stranski-Krastanov (SK) growth mode.

180 ning 24 cases (17.9%) were considered likely SKs, even by dermoscopy.

181 The cancer cell line SK-HEP-1, but not normal human umbilical vein endothelia

182 iferative efficacy in the melanoma cell line SK-MEL-2 but showed only weak antitumor activity in the

183 topic xenografts of a drug-resistant NB line SK-N-BE(2)C (mutated TP53); (iii) flank xenografts of a

184 used to transduce human melanoma cell lines SK-MEL-05 and SK-MEL-147 (both wild type p53).

185 In 3 human neuroblastoma cell lines (SK-N-AS, SK-N-BE2, and SH-SY5Y), soluble HBEGF is suffic

186 By use of human and rat neuronal cell lines (SK-N-SH and PC12), we show that overexpression of one of

187 Primary AML cells had significantly lower SK activity and intracellular S1P concentrations than co

188 We investigated an isolated maxillary M3 (SK 835) from the 1.5 to 1.8-million-year-old (Mya) site

189 -ctpfc)] toward prostate (DU-145), melanoma (SK-MEL-28), breast (MDA-MB-231), and ovarian (OVCAR-3) c

190 ffect on breast cancer (MCF-7) and melanoma (SK-MEL-5) was proven.

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

192 f multikinase networks (MKNs) where multiple SKs collaborate to detect and integrate numerous differe

193 Y79 retinoblastoma cells and CD44-negative SK-N-DZ neuroblastoma cells transduced with adenoviral v

194 levels on a non-MYCN amplified neuroblastoma SK-N-SH cell line.

195 5 in APP (APP-S675E), in human neuroblastoma SK-N-AS cells, reduces secretion of the soluble APP ecto

196 nthesized and evaluated in the neuroblastoma SK-N-FI cell line for improved targeting and to offer a

197 ured and differentiated human neuroblastoma (SK-N-SH) cells to neuronal cells with all-trans retinoic

198 drial trafficking in cultured human neuronal SK-N-SH cells and on axonal transport in mouse sciatic n

199 er, our studies also support a blunted NMDAR-SK channel coupling in MNNs of HF rats, establishing it

200 classified each dermoscopically as SK or not SK.

201 y a p53 inhibitor and marginal in a p53-null SK-N-AS cell line, suggesting dependence on p53.

202 Nevertheless, in the Oct6-SK condition many otherwise Oct4-bound locations become

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

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

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

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

207 actions were also inhibited by activation of SK channels.

208 on conductance that coupled to activation of SK channels.

209 unction are due to an enhanced activation of SK-type K(+) channels that suppresses NMDAR-dependent EP

210 st molecules induced significant adhesion of SK-MEL-24 cells and Saos-2 cells as a valuable model for

211 ach individual VGCCs, of A-type VGKCs and of SK and BK channels.

212 We also observed that blockade of SK channels potentiated NMDAR-evoked firing, and abolish

213 found that in MNNs of sham rats, blockade of SK channels with apamin (200 nM) significantly increased

214 ioning, and point toward a downregulation of SK channels as a potential underlying mechanism.

215 To describe the dermoscopic features of SK-like melanomas to understand their clinical morpholog

216 thereby maintaining the ongoing fidelity of SK-mediated inhibition in response to phasic release of

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

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

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

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

221 the Ca(2+) /voltage-dependent inhibition of SK channels without changing their sensitivity to activa

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

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

224 P waveform and developed a computer model of SK channels with rectification features.

225 esis that post-translational modification of SK channels under conditions accompanied by enhanced adr

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

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

228 nism underlies the functional recruitment of SK channels not only in cardiac disease, but also in nor

229 Consistent with this prediction, rescue of SK responses by subthreshold depolarization required the

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

231 increased mRNA levels for the SK3 subunit of SK-type K(+) channels in ventral pyramidal cells is asso

232 In conclusion, upregulation of SK channels in diseased VMs is mediated by hyperadrenerg

233 Intact explants of SKs were also sensitive to Akt inhibition.

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

235 ue-white veil, despite the presence of other SK features, allows the correct diagnosis of most of the

236 nsitivity of the channels by phosphorylating SK-bound calmodulin.

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

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

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

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

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

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

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

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

245 all conductance Ca(2+) -activated potassium (SK) current (ISK ).

246 all conductance calcium-activated potassium (SK)-channel dysfunction causes hippocampal neuron hypere

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

248 mall-conductance Ca(2+)-activated potassium (SKs) channels.

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

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

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

252 d 0.30 for R:SN , 0.36 for R:SP , 0.32 for R:SK , 0.27 for R:SCa , and 0.35 for R:SMg , respectively.

253 ate that SKIP down-regulation in AML reduces SK activity and ceramide levels, an effect that ultimate

254 differentiated SH-SY5Y cells and the related SK-N-SH cell line.

255 Further, rescued SK responses were time-locked to ACh application, rather

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

257 Intracellular application of selective SK-channel openers or a genetic reintroduction of an N-t

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

259 These simple pathways with only a single SK are not well suited to making complex decisions where

260 ), p-cresol (p-C), indole (ID), and skatole (SK)).

261 chyma cells (PC), stone cells (ST) and skin (SK) at ripe and overripe stage were characterized using

262 amin in vitro, we show that blocking somatic SK channels enhances action potential output, whereas bl

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

264 ed outward current sensitive to the specific SK inhibitor apamin (100 nmol L(-1) ), which was elimina

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

266 mmatory response, and examined ear swelling, SK activity, vascular permeability, leukocyte recruitmen

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

268 Moreover, we find that SK-dependent intrinsic plasticity is occluded in conditi

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

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

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

272 The SK-current defect was mediated, at least in part, by los

273 Moreover, although the SK blocker apamin (200 nm) strengthened the input-output

274 nels are activated solely by Ca(2+), but the SK current (I(SK)) is inwardly rectified.

275 channel activator 1-EBIO and mimicked by the SK channel blocker apamin.

276 ctor (7.2 g CO2e/kWh) is substituted for the SK grid-average electricity GHG emission factor (768 g C

277 t showed only weak antitumor activity in the SK-MEL-2 human melanoma xenograft model.

278 While ectopic expression of OPN in the SK-MES-1 lung cancer cells increased levels of cellular

279 Here, we inactivated the SK gene of the TCS MtrAB, mtrB, generating the strain De

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

281 and in vivo Using local applications of the SK channel antagonist apamin in vitro, we show that bloc

282 ating ion-channel activity, specifically the SK channels, in hyperexcitability defects in FXS.

283 Opposite effects were observed using the SK channel enhancer NS309.

284 Traditionally, QDs formed via the SK growth mode form on top of a flat wetting layer (WL)

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

286 n part, by loss of FMRP interaction with the SK channels (specifically the SK2 isoform), without chan

287 These SK-channel-dependent deficits led to markedly increased

288 This SK channel model replicates key features of I(SK) record

289 current and voltage, we identified all three SK isoforms (SK1, SK2 and SK3) in mouse SAN.

290 The addition of recombinant versican G1 to SK-N-DZ cells results in a similar activation of transge

291 tor defects, all of which are insensitive to SK pharmacological targeting and not found in the TRN-re

292 stimulates PKD2 channels in ECs, leading to SK/IK channel and eNOS activation, hyperpolarization, va

293 e a current that displayed no sensitivity to SK channel inhibitors and a decreased sensitivity to IKC

294 urrent that displayed typical sensitivity to SK channel inhibitors, while expressed IKCa channel curr

295 ne palmitoyl transferase antagonist) and two SK inhibitors (SKI-II and ABC294640).

296 Using SK-MEL 28 human melanoma cells, we show that endogenous

297 ized, CF-EPSPs mainly activate T-type VGCCs, SK channels, and A-type VGKCs that limit the transient V

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

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

300 The airway hyperresponsiveness test with SK-1211 was no specific concern with safety and useful i