ライフサイエンスコーパス: KATP channel

1 mutations in the ATP-sensitive K(+) channel (KATP channel).

2 to inhibit ATP-sensitive potassium channels (KATP channels).

3 nucleotide inhibition and activation of the KATP channel.

4 zation required the activation of a putative Katp channel.

5 pendent insulin secretion independent of the KATP channel.

6 ulfonylurea receptor 1 (SUR1) subunit of the KATP channel.

7 n participants with E23K polymorphism in the KATP channel.

8 P2, consequently reducing PIP2 activation of KATP channels.

9 PIP2 binds the Kir6.2 subunit to open KATP channels.

10 otypes that are specific for SUR1-containing KATP channels.

11 mechanism for CaMKII-dependent regulation of KATP channels.

12 new series of potent activators of vascular KATP channels.

13 pyridothiadiazine dioxides, for activity on KATP channels.

14 ions were synthesized as openers of vascular KATP channels.

15 ivate both plasma membrane and mitochondrial KATP channels.

16 -opioid receptor may be mediated via opening KATP channels.

17 of AA potently activate cardiac and vascular KATP channels.

18 sition and physiological role of endothelial KATP channels.

19 gnificantly inhibited activation of vascular KATP channels.

20 etermining the intrinsic open probability of KATP channels.

21 beta-cells in that they require both GLK and KATP channels.

22 ting the physiological activity of beta-cell KATP channels.

23 espectively, of vascular smooth muscle (VSM) KATP channels.

24 tion following expression of ATP-insensitive KATP channels.

25 eatment with pinacidil, a specific opener of KATP channels.

26 N activity was impaired due to activation of KATP channels.

27 hich phosphorylation of SUR2B NBD1 activates KATP channels.

28 bunits of the plasmalemmal ATP-sensitive K+ (KATP) channel.

29 ATP-sensitive inwardly rectifying potassium (KATP) channels.

30 ing to a closure of ATP-sensitive potassium (KATP) channels.

31 n the presence of overactive ATP-insensitive KATP channels, a reduction in Cx36 would allow elevation

32 or silencing Kir6.2, a major subunit of the KATP channel, abolished ghrelin inhibition in vitro and

33 or silencing Kir6.2, a major subunit of the KATP channel, abolished ghrelin inhibition.

34 myorelaxant activity, resulting from both a KATP channel activation and a calcium channel blocker me

35 ft ventricular pressure is closely linked to KATP channel activation and that KATP channel inhibition

36 ne can prevent severe energy deprivation and KATP channel activation in SNr neurons, active glucose m

37 s suggest that suppression of EGP by central KATP channel activation may be lost in type 2 diabetes.

38 In type 2 diabetic subjects, extrapancreatic KATP channel activation with diazoxide under fixed hormo

39 rdiac electrophysiology and vascular tone by KATP channel activation, albeit through different mechan

40 Hyperglycaemia, rather than KATP channel activation, underlies these changes, as the

41 f AP duration (APD) shortening attributed to KATP channel activation.

42 hospholipase A2 (PLA2) and ATP-sensitive K+ (KATP) channel activation whereas A2A-mediated NO release

43 erence inhibits SOCE and ATP-sensitive K(+) (KATP) channel activation.

44 K+ efflux resulting from A1-receptor-coupled KATP-channel activation facilitates Ca2+ influx which ma

45 Sarcolemmal ATP-sensitive potassium channel (KATP channel) activation in isolated cells is generally

46 f ATP-sensitive K(+) (KATP) channels, as the KATP channel activator diazoxide inhibited the effects o

47 The KATP channel activator diazoxide was administered in a r

48 In this study, we examined whether the KATP channel-activator diazoxide was able to amplify the

49 for the first time the potential utility of KATP channel activators to improve CRRs to hypoglycemia

50 A), are potent sarcolemmal ATP-sensitive K+ (KATP) channel activators.

51 We found that 1 microm AA enhanced KATP channel activities in both cardiac and vascular smo

52 amine the function of persistent PKMzeta and KATP channel activity after the preconditioning was esta

53 uence, mutant beta-cells showed less on-cell KATP channel activity and fired action potentials in glu

54 lic guanosine monophosphate (cGMP) analog on KATP channel activity and insulin secretion point to par

55 Our data indicate that SOCE and KATP channel activity are regulated by STIM1.

56 Reconstitution of KATP channel activity by coexpression of members of the

57 Our results indicate that D207E increases KATP channel activity by increasing intrinsic stability

58 B253, which reversibly and repeatedly blocks KATP channel activity following exposure to violet-blue

59 models, it was hypothesized that the loss of KATP channel activity in arterial vascular smooth muscle

60 can be achieved by genetic downregulation of KATP channel activity specifically in VSM, and by chroni

61 and aromatic substitution were evaluated for KATP channel activity using Ltk- cells stably transfecte

62 t cAMP-mediated activation of Epac modulates KATP channel activity via a Ca2+-dependent mechanism inv

63 Membrane potential and KATP channel activity were recorded using the perforated

64 howed that the R1420H substitution decreases KATP channel activity.

65 el trafficking, carbamazepine also inhibited KATP channel activity.

66 condary inhibition coinciding with increased KATP channel activity.

67 agents, which couples glucose metabolism to KATP channel activity.

68 was not mediated by ATP-sensitive potassium (KATP) channel activity, but if we lowered the perfusion

69 We have shown that treatment with the KATP channel agonist pinacidil increases survival of bee

70 5 of 16 were well controlled on diazoxide, a KATP channel agonist.

71 Replacement with tyrosine (Y) rendered the KATP channel almost completely insensitive to ATP block,

72 Thus, continuous KATP channel and PKMzeta activity are required to mainta

73 unctionality of glomeruli, cardio-protective KATP channels and adipocytes, respectively.

74 nnel openers (KCOs) activate plasma membrane KATP channels and depolarize mitochondria in several cel

75 Memantine also inhibited Kir6.1 and Kir6.2 KATP channels and elevated intracellular Ca(2+) concentr

76 Cx36 into mice that express ATP-insensitive KATP channels and measured glucose homeostasis and islet

77 anganese superoxide dismutase, mitochondrial KATP channels and peroxisome proliferator activated rece

78 ine and glibenclamide compete for binding to KATP channels, and both drugs share a binding pocket in

79 NDM) involving expression of ATP-insensitive KATP channels, and by a multi-cellular computational mod

80 Intracellular Mg(2+) regulates glucokinase, KATP channels, and L-type Ca(2+) channels in pancreatic

81 Administering a KATP channel antagonist or silencing Kir6.2, a major sub

82 Administering a KATP channel antagonist or silencing Kir6.2, a major sub

83 fection with FHV, whereas treatment with the KATP channel antagonist tolbutamide decreases survival a

84 the protonophore FCCP, or the mitochondrial KATP channel antagonist, tolbutamide.

85 Our results indicate that KATP channels are activated to a greater extent in perfu

86 KATP channels are also thought to be expressed in vascul

87 the above vascular effects, confirming that KATP channels are closely involved in the mechanism of a

88 it through different mechanisms: the cardiac KATP channels are directly activated by EETs, whereas ac

89 d wild-type mice show that Kir6.1-containing KATP channels are indeed present in vascular endothelium

90 KATP channels are inhibited by ATP (or ADP) binding to K

91 KATP channels are metabolic sensors that couple cell ene

92 rgeted against neuronal, rather than muscle, KATP channels are needed to treat the motor deficits and

93 In this work, we show that cardiac KATP channels are regulated by heme.

94 The ATP-sensitive potassium (KATP) channels are crucial for stress adaptation in the

95 ATP-sensitive potassium (KATP) channels are heteromultimeric complexes of an inwa

96 ATP-sensitive potassium (KATP) channels are widely expressed in the cardiovascula

97 2 (SUR2) subunits of the ATP-sensitive K(+) (KATP) channel as well as two mutations (V65M and C176S)

98 by activating inhibitory ATP-sensitive K(+) (KATP ) channels, as well as a class of excitatory non-se

99 required the closing of ATP-sensitive K(+) (KATP) channels, as the KATP channel activator diazoxide

100 Activation of KATP channels at the spinal level reduces pain hypersens

101 rdiovascular phenotypes by administering the KATP channel blocker glibenclamide.

102 cine were abolished by pretreatment with the KATP channel blocker glibenclamide.

103 isted in the presence of PKA inhibitors, the KATP channel blocker tolbutamide, and the L-type Ca(2+)

104 The hyperpolarization was reversed by the KATP channel blocker tolbutamide.

105 ptor agonist; b) pentazocine pretreated with KATP channel blocker, glibenclamide (0.3 mg/kg), adminis

106 st, intrathecal delivery of glibenclamide, a KATP channel blocker, or the specific Kir6.2-siRNA signi

107 When either tolbutamide, a KATP channel blocker, or ZIP were administered at least

108 Glibenclamide, a KATP channel blocker, when present only during the hypox

109 sulfonylureas tolbutamide and glibenclamide (KATP channel blockers), and diazoxide (KATP channel open

110 wer risk for hypoglycemic events compared to KATP channel blockers.

111 nhibited by the soluble guanylyl cyclase and KATP channel blockers.

112 n were attenuated by 5-HD and glibenclamide, KATP channel blockers.

113 of Cx36, after expression of ATP-insensitive KATP channels, blood glucose levels rapidly rose to >500

114 d not appear to be related to the opening of KATP channels but rather reflected a mechanism of action

115 mediates GSIS in part via ATP-regulated K+ (KATP) channels, but multiple lines of evidence suggest p

116 Here, we review the regulation of the KATP channel by adenine nucleotides and present an equil

117 mide did not alter the activation of cardiac KATP channels by 5 microm 11,12-EET, but significantly i

118 by EETs, whereas activation of the vascular KATP channels by EETs is protein kinase A dependent.

119 However, activation of cardiac and vascular KATP channels by endogenously produced EETs under physio

120 pared the activation of cardiac and vascular KATP channels by extracellularly and intracellularly app

121 adenosine triphosphate-sensitive potassium (KATP) channels by low-dose diazoxide (DZX) improves hypo

122 Because KATP channels can be activated by hydrogen peroxide (H2O

123 Loss-of-function mutations of beta-cell KATP channels cause the most severe form of congenital h

124 sine triphosphate (ATP)-sensitive potassium (KATP) channel, cause neonatal diabetes.

125 fonylurea tolbutamide, a specific blocker of KATP channels, closed KATP channels, elevated intracellu

126 cells, indicating that events downstream of KATP channel closure remained intact.

127 creases, leading to ATP-sensitive potassium (KATP) channel closure, which initiates depolarization th

128 glucose-stimulated GLP-1 secretion and that KATP-channel closure is required to stimulate a full-blo

129 how sulfonylureas and ATP interact with the KATP channel complex to inhibit channel activity.

130 potassium channel, Kir6.2 (alpha subunit of KATP channel complex), and we identify the specific resi

131 ATP-regulated potassium (KATP) channel complexes of inward rectifier potassium ch

132 edications that act by inhibiting pancreatic KATP channels composed of SUR1 and Kir6.2.

133 ogenesis defects in ATP-sensitive potassium (KATP) channels composed of sulfonylurea receptor 1 (SUR1

134 ATP-sensitive potassium (KATP) channels comprise four pore-forming Kir6.2 subunit

135 nced sensitivity is driven by a reduction in KATP channel conductance (diazoxide: young 5.1 +/- 0.2 n

136 es, inhibits insulin secretion by increasing KATP channel conductance in beta-cells.

137 ated the mechanism by which leptin increases KATP channel conductance.

138 ATP-sensitive potassium (KATP) channels consisting of sulfonylurea receptor 1 (SU

139 d the effect of the Kir6.2-F333I mutation on KATP channels containing SUR1, SUR2A or SUR2B.

140 esent two structures of the human pancreatic KATP channel, containing the ABC transporter SUR1 and th

141 The beta-cell ATP-sensitive potassium (KATP) channel controls insulin secretion by linking gluc

142 Next, Syn-1A.SUR1 complex modulation of KATP channels could be observed at a physiologically low

143 ATP-sensitive potassium (KATP) channels couple cell metabolism to electrical acti

144 ATP-sensitive potassium (KATP) channels couple the metabolic status of a cell to

145 The ATP-sensitive K+ channel (KATP channel) couples glucose metabolism to insulin secr

146 the result of reciprocal actions on VRAC and KATP channel currents, and could contribute towards the

147 vely potentiate secretion in islets from the KATP channel-deficient mice and in other models of KATP

148 Mechanistically, glucose triggers KATP channel-dependent calcium signaling, which promotes

149 gulator of both the ATP-regulated potassium (KATP) channel-dependent and -independent pathways of ins

150 KATP channels do not drive this, as tolbutamide did not

151 a specific blocker of KATP channels, closed KATP channels, elevated intracellular calcium levels, an

152 llular nucleotides, ATP-sensitive potassium (KATP) channels exhibit spontaneous activity via a phosph

153 MgADP, and the sulphonylurea gliclazide with KATP channels expressed in Xenopus oocytes.

154 lecule corrector that may be used to restore KATP channel expression and function in a subset of cong

155 Our findings suggest that the KATP channel expression level in the spinal cord is redu

156 ether adenosine triphosphate-sensitive K(+) (KATP) channel expression relates to mechanical and hypox

157 l cyclase/cGMP signaling triggers opening of KATP channels for vasodilation.

158 veal a novel molecular mechanism for loss of KATP channel function and congenital hyperinsulinism and

159 Loss of KATP channel function due to mutations in ABCC8 or KCNJ1

160 Loss of KATP channel function due to mutations in ABCC8 or KCNJ1

161 uable research tool for the interrogation of KATP channel function in health and T2DM.

162 sponsible for CaMKII-dependent regulation of KATP channel function.

163 ound for investigating beta-cell physiology, KATP channel gating, and a new chemical scaffold for dev

164 Loss-of-function mutations in the KATP channel genes KCNJ11 and ABCC8 cause neonatal hyper

165 These findings demonstrate that VSM KATP channel GoF underlies CS cardiac enlargement and th

166 he KIR6.2 and SUR1 subunits of the beta-cell KATP channel, have previously been implicated in type 2

167 HI-D) arises from mutations inactivating the KATP channel; however, the phenotype is difficult to exp

168 glibenclamide, implicating ATP-sensitive K+ (KATP) channels; however, tissue ATP was unaltered.

169 es significant insight into the roles of the KATP channel in the cardiovascular system and suggests n

170 of the mechanisms whereby EETs activate the KATP channels in cardiac myocytes versus vascular smooth

171 cal microscopy to examine the involvement of KATP channels in cardioprotection afforded by preconditi

172 this study, we examined the effects of AA on KATP channels in freshly isolated cardiac myocytes from

173 DMR is due to the activation of SUR2/Kir6.2 KATP channels in HepG2C3A cells.

174 esent study demonstrate the critical role of KATP channels in modulating myocardial function over a w

175 This was due to a reduced sensitivity of KATP channels in pancreatic beta cells to inhibition by

176 m suppressed insulin secretion by overactive KATP channels in pancreatic beta-cells, but the source o

177 We determined the role of spinal KATP channels in the control of mechanical hypersensitiv

178 athophysiological roles ascribed to arterial KATP channels in the control of vascular tone and blood

179 lar smooth muscle cells; whether ADO acts on KATP channels in these resistance vessels; and the contr

180 KATP channels in vascular smooth muscle have a well-defi

181 Despite successful restoration of KATP channels in vascular smooth muscle, transgene-resto

182 to generate mice that restored expression of KATP channels in vascular smooth muscle.

183 Understanding the activation of KATP channels in working myocardium during high-stress s

184 ctivating mutations of the ATP-sensitive K+ (KATP) channel in the pancreatic beta cell.

185 /SUR2A (i.e., the principal ventricular-type KATP) channels in HEK293 cells, whereas the increase was

186 et al. explore the role of ATP-sensitive K+ (KATP) channels in maintaining glucose homeostasis.

187 rding currents from ATP-sensitive potassium (KATP) channels in single cells, showing that PercevalHR

188 gulatory subunit of ATP-sensitive potassium (KATP) channels in vascular smooth muscle.

189 arcolemmal ATP-sensitive potassium channels (KATP channels) in cardiac myocytes adjust contractile fu

190 r6.2 subunit of the ATP-sensitive potassium (KATP) channel, in a patient with transient neonatal diab

191 ne segment (TM2) to proline in Kir6.2 causes KATP channel inactivation.

192 to its active form, leading to an increased KATP channel-induced hyperpolarizaton.

193 effect by binding to the SUR1 subunit of the KATP channels inducing insulin secretion in beta-cells.

194 KATP channel inhibition by MgATP was enhanced in both ho

195 As a result, KATP channel inhibition probably exacerbates a mismatch

196 y linked to KATP channel activation and that KATP channel inhibition with a low concentration of tolb

197 ation alters channel regulation resulting in KATP channel inhibition, a cellular phenotype consistent

198 hronic administration of the clinically used KATP channel inhibitor, glibenclamide.

199 Cross-linking experiments showed that KATP channel inhibitors promoted interactions between th

200 ed whether the actions of PIP2 on activating KATP channels is contributed by sequestering Syn-1A from

201 The effect of leptin on KATP channels is dependent on the protein kinases AMP-ac

202 eviously been suggested that the function of KATP channels is modulated by nitric oxide (NO), a gaseo

203 UR1) subunit of the ATP-sensitive potassium (KATP) channel is a member of the ATP-binding cassette (A

204 In persistently depolarized beta cells from KATP channel knockout (KO) mice, the researchers reveale

205 ar to increase ATP/ADP ratio that blocks the KATP channel leading to membrane depolarization and insu

206 Cs to produce vasodilation via activation of KATP channels located on vascular smooth muscle cells.

207 ATP-sensitive potassium (KATP) channels may be involved in regulating nociceptive

208 Activated PKG opens mitochondrial KATP channels (mitoKATP) which increase production of re

209 optimal scaffold for activators of vascular KATP channels; moreover, the high level of potency exhib

210 ll-specific expression of a human activating KATP channel mutation in adult mice leads to rapid diabe

211 drome (CS), which is a result of one kind of KATP channel mutation.

212 applied this model to predict how different KATP channel mutations found in NDM suppress [Ca2+], and

213 anylyl cyclase, and ATP-sensitive potassium (KATP) channels nearly abolished lactate-induced vasodila

214 ing Cx36 after expression of ATP-insensitive KATP channels, normal glucose levels were maintained.

215 r indicate that PIP2 affects islet beta-cell KATP channels not only by its actions on Kir6.2 but also

216 glucose concentration monitors the gating of KATP channels of sleep-promoting neurons, highlighting t

217 tudy of coordinated variation in ATP:ADP and KATP channel open probability in intact cells.

218 This study evaluated the hypothesis that a KATP channel opener (diazoxide) would benefit volume hom

219 e phosphate and dipeptide derivatives of the KATP channel opener cromakalim and evaluated their IOP l

220 Importantly, combination of the KATP channel opener diazoxide and carbamazepine led to e

221 The KATP channel opener diazoxide is used clinically to trea

222 .9T, and 0.6T) solutions with or without the KATP channel opener diazoxide.

223 reas or carbamazepine was facilitated by the KATP channel opener diazoxide.

224 lium-dependent vasorelaxation induced by the KATP channel opener pinacidil.

225 mide (KATP channel blockers), and diazoxide (KATP channel opener).

226 Intrathecal injection of pinacidil, a KATP channel opener, significantly increased the tactile

227 adenosine triphosphate-sensitive potassium (KATP) channel opener.

228 which we clamped membrane potential with the KATP channel-opener diazoxide and KCl to fix Ca(2+) at a

229 e PKG induces opening of mitoKATP similar to KATP channel openers like diazoxide and cromakalim in he

230 These data indicate that KATP channel openers regulate arterial diameter via SUR-

231 none of the mutant channels were rescued by KATP channel openers.

232 y, antihypertensive ATP-sensitive potassium (KATP) channel openers (KCOs) activate plasma membrane KA

233 ATP-sensitive K+ (KATP) channel openers are vasodilators that activate bot

234 ATP-sensitive potassium (KATP) channel openers have emerged as potential therapeu

235 e reference ATP-sensitive potassium channel (KATP channel) openers diazoxide and 7-chloro-3-isopropyl

236 Inhibition of KATP channels or increasing interstitial potassium by di

237 ng adenosine triphosphate (ATP)-sensitive K (KATP) channels or activation of delta-opioid receptors m

238 bited P2Y receptors, adenosine receptors, or KATP channels; or (3) inhibited downstream signaling pat

239 tify locomotor hyperactivity as a feature of KATP channel overactivity.

240 Diazoxide (250 microm), an activator of KATP channels, paradoxically potentiated glucose-stimula

241 Finally, we demonstrate aberrant KATP channel phosphorylation in betaIV-spectrin mutant m

242 The KATP channels play a vital role in preserving the metabo

243 ATP-sensitive potassium (KATP) channels play a key role in mediating glucose-stim

244 ATP-sensitive potassium (KATP) channels play a prominent role in controlling card

245 itochondrial (mito) ATP-sensitive potassium (KATP) channels play crucial roles in excitability and ca

246 The data imply that endocytosis of KATP channels plays a crucial role in the (patho)-physio

247 ng to NBD2 is translated into opening of the KATP channel pore.

248 t of the drug memantine, ATP-sensitive K(+) (KATP) channels, potentially relevant to memory improveme

249 , corrects the trafficking defects of mutant KATP channels previously identified in congenital hyperi

250 Our results suggest that KATP channels provide a significant link between cellula

251 sculature, ATP-sensitive potassium channels (KATP) channels regulate vascular tone.

252 nd SUR2 subunits of ATP-sensitive potassium (KATP) channels, respectively.

253 In many excitable cells, KATP channels respond to intracellular adenosine nucleot

254 that the leptin-induced increase in surface KATP channels results in more hyperpolarized membrane po

255 ectrical excitability and is crucial for the KATP channel's role in regulating insulin secretion, car

256 GLUT2 may act after metabolization, closing KATP channels similar to sulfonylureas, which also stimu

257 ility of PIP2 to stabilize the open state of KATP channels, similar to mutations in the cytoplasmic d

258 intact cardiomyocytes, but the H2O2-induced KATP channel stimulation was obliterated when ERK1/2 or

259 etagogues and was mediated by alterations in KATP channel subunit expression and activity.

260 o had 6q24 abnormalities versus mutations in KATP channel subunit genes (82% vs 86%; p=0.36).

261 1-15) in 27 index patients with mutations in KATP channel subunit genes who did not have developmenta

262 red with index patients who had mutations in KATP channel subunit genes, those with 6q24 abnormalitie

263 In contrast, SUR1, a KATP channel subunit, was expressed in GE and some NR ce

264 We assessed changes in the 6q24 locus, KATP-channel subunit genes (ABCC8 and KCNJ11), and prepr

265 articipants with mutations in genes encoding KATP channel subunits).

266 (Kir6.1, KCNJ8) and accessory (SUR2, ABCC9) KATP channel subunits.

267 mplex with vascular ATP-sensitive potassium (KATP) channel subunits and that cAMP-mediated activation

268 gh their actions on ATP-sensitive potassium (KATP) channels, sulfonylureas boost insulin release from

269 tivation of central ATP-sensitive potassium (KATP) channels suppresses EGP in nondiabetic rodents and

270 -cells but not beta-cells lacking functional KATP channels (SUR1-KO), ANP increased electrical activi

271 data support the existence of an endothelial KATP channel that contains Kir6.1, is involved in vascul

272 have identified activating mutations in the KATP channel that prevent its closure and hence insulin

273 clusters to bind SUR1, causing inhibition of KATP channels that could no longer be further inhibited

274 nder the control of ATP-sensitive potassium (KATP) channels that play key roles in setting beta-cell

275 Mutations to the ATP-sensitive K(+) channel (KATP channel) that reduce the sensitivity of ATP inhibit

276 s in Kir6.2, the pore-forming subunit of the KATP channel, that reduce the ability of ATP to block th

277 al signals activate ATP-sensitive potassium (KATP) channels, thereby down-regulating glucose producti

278 an inhibitor of the ATP-dependent potassium (KATP)-channels, thus suggesting a possible mechanism und

279 This dual regulation enables the KATP channel to couple the metabolic state of a cell to

280 ed that activity-generated H2 O2 can act via KATP channels to inhibit dopamine release in dorsal stri

281 king Abcc8, a key component of the beta-cell KATP-channel, to analyze the effects of a sustained elev

282 ding diseases, carbamazepine did not correct KATP channel trafficking defects by activating autophagy

283 Our study expands the list of KATP channel trafficking mutations whose function can be

284 cellular mechanism by which leptin regulates KATP channel trafficking to modulate beta-cell function

285 f F-actin simulates, the effect of leptin on KATP channel trafficking, indicating that leptin-induced

286 nockdown showed that the pinacidil activated KATP channels trigger signaling through Rho kinase and J

287 rements in islets expressing ATP-insensitive KATP channels under different levels of gap junction cou

288 Here, we report that KATP channels undergo rapid internalisation from the pla

289 It is generally believed that closure of KATP channels underlies the depolarizing action of gluco

290 corrector effect of carbamazepine on mutant KATP channels was also demonstrated in rat and human bet

291 ion mediated by the ATP-sensitive potassium (KATP) channel, was decreased in betaLPL-TG islets but in

292 n flow rate or omitted the alternative fuel, KATP channels were activated and could silence SNr firin

293 ing rabbit hearts to assess when sarcolemmal KATP channels were activated during physiologically rele

294 ATP-sensitive potassium (KATP) channels were first discovered in the heart 30 yea

295 ported recently for ATP-sensitive potassium (KATP) channels, which are critical for coupling glucose

296 ATP and ADP, which have opposing actions on KATP channels, with ATP closing and MgADP opening the ch

297 ATP-sensitive potassium (KATP) channels within the hypothalamus are thought to be

298 transient increase in surface expression of KATP channels without affecting channel gating propertie

299 cause functional DA denervation via H2O2 and KATP channels, without DA or ATP depletion.

300 resultant increase in the surface density of KATP channels would predispose beta-cells to hyperpolari