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 all four Kir6.2 subunit inner helices of the KATP channel.

7 l role of ATP in metabolic regulation of the KATP channel.

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

9 n participants with E23K polymorphism in the KATP channel.

10 P2, consequently reducing PIP2 activation of KATP channels.

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

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

13 mechanism for CaMKII-dependent regulation of KATP channels.

14 sition and physiological role of endothelial KATP channels.

15 new series of potent activators of vascular KATP channels.

16 pyridothiadiazine dioxides, for activity on KATP channels.

17 ions were synthesized as openers of vascular KATP channels.

18 ivate both plasma membrane and mitochondrial KATP channels.

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

20 of AA potently activate cardiac and vascular KATP channels.

21 gnificantly inhibited activation of vascular KATP channels.

22 etermining the intrinsic open probability of KATP channels.

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

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

25 tion following expression of ATP-insensitive KATP channels.

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

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

28 hich phosphorylation of SUR2B NBD1 activates KATP channels.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

48 The KATP channel activator diazoxide was administered in a r

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

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

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

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

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

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

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

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

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

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

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

60 In the heart, KATP channel activity has been linked to homeostatic sho

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

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

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

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

65 ism(s) by which glucose metabolism regulates KATP channel activity, however, remains controversial.

66 el trafficking, carbamazepine also inhibited KATP channel activity.

67 condary inhibition coinciding with increased KATP channel activity.

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

69 howed that the R1420H substitution decreases KATP channel activity.

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

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

72 5 of 16 were well controlled on diazoxide, a KATP channel agonist.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

87 Experiments with different antagonists of KATP channels, applied at different times during the exp

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

89 KATP channels are also thought to be expressed in vascul

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

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

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

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

94 KATP channels are metabolic sensors that couple cell ene

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

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

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

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

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

100 2 (SUR2) subunits of the ATP-sensitive K(+) (KATP) channel as well as two mutations (V65M and C176S)

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

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

103 l, suggested that the opening of sarcolemmal KATP channels at the beginning of sustained hypoxia medi

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

188 lemmal and mitochondrial ATP-sensitive K(+) (KATP) channels in the heart is believed to mediate ische

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

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

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

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

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

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

195 KATP channel inhibition by MgATP was enhanced in both ho

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

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

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

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 Closure of ATP-sensitive K+ channels (KATP channels) is a key step in glucose-stimulated insul

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

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

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

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

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

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

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

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

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

220 The KATP channel opener diazoxide is used clinically to trea

221 .9T, and 0.6T) solutions with or without the KATP channel opener diazoxide.

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

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

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

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

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

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

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

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

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

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

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

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

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

235 Inhibition of KATP channels or increasing interstitial potassium by di

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

260 1-15) in 27 index patients with mutations in KATP channel subunit genes who did not have developmenta

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

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

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

264 Inhibition of trafficking of KATP channel subunits prevented preconditioning without

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