ライフサイエンスコーパス: mitoK(ATP)

1 others in the mitochondrial inner membrane (mitoK(ATP)).

2 he mitochondrial ATP-sensitive K(+) channel (mitoK(ATP)).

3 (PKG), and the mitochondrial K(ATP) channel (mitoK(ATP)).

4 similar to or different from those of heart mitoK(ATP).

5 x in liposomes containing partially purified mitoK(ATP).

6 association of mitochondrial PKC epsilon and mitoK(ATP).

7 Preconditioning protects the heart through mitoK(ATP).

8 found that inhibition of GSK3beta activated mitoK(ATP).

9 azoxide produces delayed preconditioning via mitoK(ATP) activation but that physiological status can

10 is channel activity is sensitive not only to mitoK(ATP) activators and blockers but also to SDH inhib

11 uccinate dehydrogenase (SDH) is inhibited by mitoK(ATP) activators, fueling the contrary view that SD

12 h-affinity ROMK toxin, tertiapin Q, inhibits mitoK(ATP) activity in isolated mitochondria and in digi

13 Flavoprotein fluorescence, a marker of mitoK(ATP) activity, is higher in cardiomyocytes from CY

14 that could be unequivocally associated with mitoKATP activity.

15 zoxide were reproduced by pinacidil, another mitoK(ATP) agonist, and blocked by the mitoK(ATP) channe

16 ereas diazoxide (10 micromol/L), a selective mitoK(ATP) agonist, significantly increased channel acti

17 ction and show that different open states of mitoKATP, although catalyzing identical K+ fluxes, exhib

18 s in understanding the physiological role of mitoK(ATP) and highlights outstanding questions and cont

19 this cardioprotection involves activation of mitoK(ATP) and p42/p44 MAPK.

20 a 10-fold higher concentration recruits both mitoK(ATP) and surfaceK(ATP) channels.

21 s signaling pathway, one in association with mitoK(ATP) and the other in association with MPT.

22 lux in liposomes reconstituted with purified mitoKATP and found that guanine nucleotides are potent a

23 ochondrial ATP-sensitive potassium channels (mitoK(ATP)) and protects neurons in vivo and in vitro ag

24 on, but the relative roles of mitochondrial (mitoK(ATP)) and sarcolemmal (surfaceK(ATP)) channels rem

25 cts were blocked completely by the selective mitoK(ATP) antagonist 5-hydroxydecanoate.

26 te (5-HD, 10 to 100 micromol/L), a selective mitoK(ATP) antagonist, reduced the open state probabilit

27 MitoKATP are opened by the PKC activator 12-phorbol 13-m

28 by demonstrating that SDH is a component of mitoK(ATP) as part of a macromolecular supercomplex.

29 This raises the question, how can mitoKATP be opened in the presence of physiological conc

30 On the other hand, mitoKATP became highly sensitive to glyburide and 5-HD w

31 Administration of the mitoK(ATP) blocker 5-hydroxydecanoate attenuated this be

32 P-sensitive mitochondrial potassium channel (mitoKATP) blocker 5-hydroxydecanoate.

33 respiration, and we estimated the amount of mitoK(ATP) by means of green fluorescence probe BODIPY-F

34 Inhibition of mitoKATP by long-chain acyl-CoA esters, like that of ATP

35 luate the evidence for the existence of this mitoKATP by measuring changes in light scattering (A520)

36 ted with diazoxide, a specific opener of the mitoK(ATP) channel (7 mg/kg, IV), 12, 24, 48, and 72 hou

37 Based on our recent observation that mitoK(ATP) channel activation has a remarkable antiapopt

38 onal recovery, these results may explain how mitoK(ATP) channel activation mimics ischemic preconditi

39 Using mitochondrial oxidation to index mitoK(ATP) channel activity in rabbit ventricular myocyt

40 Under these conditions, mitoK(ATP) channel activity strongly regulated Deltapsi(

41 lls, indicating that the diazoxide-sensitive mitoK(ATP) channel activity was associated with 130-kDa-

42 -induced flavoprotein oxidation, an index of mitoK(ATP) channel activity.

43 somes and lipid bilayers and shown to confer mitoK(ATP) channel activity.

44 simulate ischemic conditions, the selective mitoK(ATP) channel agonist diazoxide (25-50 microM) pote

45 ocytes were measured simultaneously to assay mitoK(ATP) channel and surface K(ATP) channel activities

46 other mitoK(ATP) agonist, and blocked by the mitoK(ATP) channel antagonist 5-hydroxydecanoate (500 mi

47 ese effects of diazoxide were blocked by the mitoK(ATP) channel antagonist 5-hydroxydecanoate (5HD).

48 ve effects of nicorandil were blocked by the mitoK(ATP) channel antagonist 5-hydroxydecanoate.

49 The effect of mitoK(ATP) channel appears to be dependent on the PKC-me

50 d (5-HD, 5 mg/kg IV), a relatively selective mitoK(ATP) channel blocker (56.5+/-2.7%), and chelerythr

51 e or by preconditioning was prevented by the mitoK(ATP) channel blocker 5-hydroxydecanoate (500 micro

52 Unexpectedly, treatment of hearts with the mitoK(ATP) channel blocker 5-hydroxydecanoate (5HD) at 1

53 duced oxidation was blocked by the selective mitoK(ATP) channel blocker 5-hydroxydecanoate and by the

54 cardioprotective effect was prevented by the mitoK(ATP) channel blocker 5-hydroxydecanoate but was un

55 ept that its effects were not blocked by the mitoK(ATP) channel blocker 5-hydroxydecanoate.

56 We hypothesized that the mitoK(ATP) channel contains a sulfonylurea receptor (SUR

57 Although the mitoK(ATP) channel has clearly been shown to be a distal

58 present study, we sought to characterize the mitoK(ATP) channel in the mouse brain using overlapping

59 udy tests the hypothesis that stimulation of mitoK(ATP) channel induces late PC via the protein kinas

60 These results indicate that MCC-134 is a mitoK(ATP) channel inhibitor and a surface K(ATP) channe

61 The third group of hearts was exposed to the mitoK(ATP) channel inhibitor, 5-hydroxydecanoic acid (5-

62 the sarcK(ATP) channel triggers and that the mitoK(ATP) channel is a distal effector of opioid-induce

63 a cellular model of simulated ischemia, the mitoK(ATP) channel opener diazoxide (100 micromol/L), bu

64 The mitoK(ATP) channel opener diazoxide attenuated the accum

65 We investigated the effects of mitoK(ATP) channel opener diazoxide on BBB functions dur

66 The mitoK(ATP) channel opener, diazoxide (50 microM), caused

67 lic inhibitor, sodium cyanide (NaCN), or the mitoK(ATP) channel opener, diazoxide.

68 amined whether both metabolic inhibition and mitoK(ATP) channel openers protect both the whole organ

69 mitochondrial redox potential as an index of mitoK(ATP) channel opening in rabbit ventricular myocyte

70 In conclusion, activation of mitoK(ATP) channel with diazoxide produces late PC again

71 e pore-forming subunit of the cytoprotective mitoK(ATP) channel.

72 ndrial matrix redox potential as an index of mitoKATP channel activity in rabbit ventricular myocytes

73 The effects of the MitoKATP channel and other interventions on functional,

74 These effects of PMA were blocked by the mitoKATP channel blocker 5-hydroxydecanoate, which we ve

75 5-hydroxydecanoate (5HD; 500 micromol/l), a mitoKATP channel blocker.

76 nd such cardioprotection can be prevented by mitoKATP channel blockers.

77 hether the potent and specific opener of the MitoKATP channel diazoxide attenuates the lethal injury

78 we verified to be a selective blocker of the mitoKATP channel in simultaneous recordings of membrane

79 ion of sodium 5-hydroxydecanoate, a specific MitoKATP channel inhibitor, or chelerythrine chloride, a

80 This study suggests that the effect of the MitoKATP channel is mediated by PKC-mediated signaling p

81 The mitoKATP channel opener diazoxide (100 micromol/L) parti

82 Potentiation of mitoKATP channel opening by PKC provides a direct mechan

83 -sensitive mitochondrial potassium channels (MitoKATP channel) are a major contributor to the cardiac

84 the existence of a sulphonylurea-inhibitable mitoKATP channel.

85 The mitochondrial K(ATP) (mitoK(ATP)) channel has been shown to confer short- and

86 Activation of mitochondrial K(ATP) (mitoK(ATP)) channel induces acute ischemic preconditioni

87 The mitochondrial ATP-sensitive potassium (mitoK(ATP)) channel opener diazoxide markedly decreased

88 The mitochondrial ATP-sensitive K(+) (mitoK(ATP)) channel plays a central role in protection o

89 This potency is similar to that for block of mitoK(ATP) channels (IC(50) = 95 microM).

90 We probed the relationship between mitoK(ATP) channels and apoptosis in cultured neonatal r

91 s of PKC downregulation on the activation of mitoK(ATP) channels and other interventions on hemodynam

92 ocardium, the location of PKB in relation to mitoK(ATP) channels and p38 mitogen-activated protein ki

93 NO directly activates mitoK(ATP) channels and potentiates the ability of diazo

94 ve signaling through mitochondrial Cx43 onto mitoK(ATP) channels and that Cx43 functions as a channel

95 Furthermore, mitoK(ATP) channels and the MPT differentially affect mi

96 The links between NO and mitoK(ATP) channels are unknown.

97 The results also pinpoint mitoK(ATP) channels as logical therapeutic targets in di

98 s revealed that PKB is located downstream of mitoK(ATP) channels but upstream of p38 MAPK.

99 Pharmacological opening of mitoK(ATP) channels by diazoxide (100 micromol/L) preser

100 It is concluded that myocardial mitoK(ATP) channels can be reconstituted into lipid bila

101 Selective activation of mitoK(ATP) channels can protect the brain or cultured ne

102 Our results demonstrate that mitoK(ATP) channels closely resemble Kir6.1/SUR1 sK(ATP)

103 ted hearts, protection was abolished because mitoK(ATP) channels could not be activated by diazoxide.

104 KC activation is required for the opening of mitoK(ATP) channels during protection against ischemia a

105 In the present study, mitoK(ATP) channels from bovine ventricular myocardium w

106 association between PKC or its isoforms and mitoK(ATP) channels has not yet been clarified.

107 c myocytes, and confirm the critical role of mitoK(ATP) channels in inhibiting apoptosis.

108 ) channel opener P-1075 on surfaceK(ATP) and mitoK(ATP) channels in rabbit ventricular myocytes.

109 5HD and diazoxide as specific modulators of mitoK(ATP) channels in the heart.

110 Unfortunately, the molecular structure of mitoK(ATP) channels is unknown, in contrast to sK(ATP) c

111 Cardiac mitoK(ATP) channels play a pivotal role in ischemic prec

112 ther support for the emerging consensus that mitoK(ATP) channels rather than surfaceK(ATP) channels a

113 ever, the intracellular mechanism regulating mitoK(ATP) channels remains unclear.

114 ly affect mitochondrial calcium homeostasis: mitoK(ATP) channels suppress calcium accumulation during

115 Activation of mitoK(ATP) channels suppresses the cell death process at

116 inhibition increased the open probability of mitoK(ATP) channels through GSK3beta, and this GSK3beta

117 RRNYRRNY activated mitoK(ATP) channels via Cx43.

118 compared the pharmacology of native cardiac mitoK(ATP) channels with that of molecularly defined sK(

119 , we found that pinacidil and diazoxide open mitoK(ATP) channels, but P-1075 does not.

120 ial mitochondrial membrane depolarization by mitoK(ATP) channels, underlies cardioprotection.

121 s a means of probing the molecular makeup of mitoK(ATP) channels, we compared the pharmacology of nat

122 To index mitoK(ATP) channels, we measured mitochondrial flavoprot

123 trations as low as 10 micromol/liter turn on mitoK(ATP) channels, while surfaceK(ATP) current require

124 important for cardiac protection elicited by mitoK(ATP) channels.

125 ecanoic acid (5HD), but not HMR-1098, blocks mitoK(ATP) channels.

126 n effect mediated by selective activation of mitoK(ATP) channels.

127 inks between NO-induced cardioprotection and mitoK(ATP) channels.

128 tangible clue as to the structural basis of mitoK(ATP) channels.

129 th FP15 has a similar effect to blocking the mitoK(ATP) channels.

130 ion also protects mitochondria by activating mitoK(ATP) channels.

131 34, opens surface K(ATP) channels but blocks mitoK(ATP) channels; the fact that this drug inhibits pr

132 g system, resulted in a marked activation of mitoK(ATP) channels; the NPo of the channels was increas

133 l openers of mitochondrial ATP-dependent K+ (mitoKATP) channels mimic ischemic preconditioning, and s

134 ecular identity of these mitochondrial KATP (mitoKATP) channels remains unclear.

135 on of mitochondrial ATP-sensitive potassium (mitoKATP) channels underlies this effect.

136 Glibenclamide's effects on mitoKATP channels are difficult to assess, because it in

137 y and subcellular localization indicate that mitoKATP channels are distinct from surface KATP channel

138 ventricular myocytes, contrasts with that of mitoKATP channels as indexed by flavoprotein oxidation.

139 We conclude that the activity of mitoKATP channels can be regulated by PKC in intact hear

140 ed a pharmacological approach to distinguish mitoKATP channels from classical, molecularly defined ca

141 MitoKATP channels in myocytes are activated equally by 1

142 -hydroxydecanoate is an effective blocker of mitoKATP channels.

143 nti-apoptotic effects in neurons mediated by mitoKATP channels.

144 ether protection by diazoxide is mediated by MitoKATP channels; whether diazoxide mimics the effects

145 oning, and mitochondrial ATP-dependent K(+) (mitoK(ATP)) channels are the likely effectors.

146 ce K(ATP) channels and mitochondrial K(ATP) (mitoK(ATP)) channels are unknown.

147 Mitochondrial ATP-sensitive potassium (mitoK(ATP)) channels have been suggested as triggers and

148 ing a primary role for mitochondrial K(ATP) (mitoK(ATP)) channels in early and delayed cardioprotecti

149 implicated opening of mitochondrial K(ATP) (mitoK(ATP)) channels in ischaemic preconditioning (IPC).

150 Mitochondrial ATP-sensitive K (mitoK(ATP)) channels play a central role in protecting t

151 Mitochondrial ATP-sensitive potassium (mitoK(ATP)) channels play a key role in ischemic precond

152 on of mitochondrial ATP-sensitive potassium (mitoK(ATP)) channels prevents lethal ischemic injury in

153 preconditioning, while mitochondrial K(ATP) (mitoK(ATP)) channels rather than sarcolemmal K(ATP) (sur

154 drial adenosine triphosphate-sensitive K(+) (mitoK(ATP)) channels, and mitochondrial connexin 43 (Cx4

155 after the discovery of mitochondrial K(ATP) (mitoK(ATP)) channels, progress has been remarkable, but

156 ivate ATP sensitive mitochondrial potassium (mitoK(ATP)) channels.

157 on of mitochondrial ATP-sensitive potassium (mitoK(ATP)) channels.

158 silon receptor for activated C kinase caused mitoK(ATP)-dependent inhibition of MPT opening.

159 ide agonist, psi epsilonRACK, each activated mitoK(ATP)-dependent K+ flux in the reconstituted system

160 However, it is not known whether mitoK(ATP) exists in brain mitochondria, and, if so, whe

161 ide labeling of the sulfonylurea receptor of mitoK(ATP) from brain and liver.

162 d by the same ligands as those that regulate mitoK(ATP) from heart and liver.

163 ial purification and reconstitution of a new mitoK(ATP) from rat brain mitochondria.

164 Here, we report that SDH forms part of mitoK(ATP) functionally and structurally.

165 To re-evaluate a functional role for the mitoKATP in brain, we used Percoll-gradient-purified bra

166 These results are consistent with a role for mitoKATP in cardioprotection and show that different ope

167 the biological roles and use of sarcKATP and mitoKATP in hESC-VCM.

168 myristate 13-acetate or H(2)O(2) resulted in mitoK(ATP)-independent inhibition of MPT opening, wherea

169 tagonist, epsilonV(1-2), and by the specific mitoK(ATP) inhibitor 5-hydroxydecanoate.

170 nclamide (GLIB) or the mitochondrial K(ATP) (mitoK(ATP)) inhibitor 5-hydroxydecanoate (5-HD) for 20 m

171 This effect was blocked by mitoKATP inhibitors 5-hydroxydecanoate, tetraphenylphosp

172 We hypothesized that PKC epsilon and mitoK(ATP) interact directly to form functional signalin

173 flux in proteoliposomes and found that brain mitoK(ATP) is regulated by the same ligands as those tha

174 The mitochondrial KATP channel (mitoKATP) is highly sensitive to ATP, which inhibits K+

175 The mitochondrial KATP channel (mitoKATP) is hypothesized to be the receptor for the car

176 We show that mitoKATP is completely insensitive to glyburide and 5-HD

177 ling the contrary view that SDH, rather than mitoK(ATP), is the target of cardioprotective drugs.

178 adenosine triphosphate-sensitive K+ channel (mitoKATP), is an important effector of protection agains

179 nnel openers, and it has been suggested that mitoK(ATP) may also play a key role in brain protection.

180 , indicating that mitochondrial Cx43- and/or mitoK(ATP)-mediated reduction of infarct size was not un

181 1/2 values 45-75 microM) inhibited specific, mitoKATP-mediated K+ flux in both heart and liver mitoch

182 examined the effects of opening and closing mitoK(ATP) on brain mitochondrial respiration, and we es

183 channel with glibenclamide and the specific mitoK(ATP) openers diazoxide and BMS-191095.

184 n vivo and in vitro, however, the effects of mitoK(ATP) openers on cerebral endothelial cells and on

185 which was reversed by the application of the mitoK(ATP) openers.

186 e notion that GSK3beta inhibition results in mitoK(ATP) opening via mitochondrial Cx43.

187 Steps between PKG and mitoKATP opening are unknown.

188 mitochondria contain six to seven times more mitoK(ATP) per milligram of mitochondrial protein than l

189 the mitochondrial ATP-sensitive K+ channel (mitoK(ATP)) plays a crucial role in originating and tran

190 ochondrial ATP-sensitive potassium channels (mitoK(ATP)) protects neuronal tissues in vivo and in vit

191 its preconditioning reaffirms the primacy of mitoK(ATP) rather than surface K(ATP), channels in the m

192 the mitochondrial ATP-sensitive K+ channel (mitoKATP) sensitive to diazoxide and 5-hydroxydecanoate

193 n) has been identified as a component of the mitoK(ATP) signaling cascade.

194 measurements indicate PKG induces opening of mitoKATP similar to KATP channel openers like diazoxide

195 de explicit evidence for the presence of the mitoKATP, similar to the cellKATP, in brain mitochondria

196 For mitoK(ATP), structural information is lacking, but there

197 nylurea-sensitive, ATP-sensitive K+ channel (mitoKATP) that is selectively inhibited by 5-hydroxydeca

198 im, minoxidil, testosterone) of the putative mitoKATP were applied to show the role of the channel in

199 vated PKG opens mitochondrial KATP channels (mitoKATP) which increase production of reactive oxygen s

200 is study, we explored the pathway that links mitoK(ATP) with the MPT.

201 -CoA inhibited K+ flux through reconstituted mitoKATP with K1/2 values of 260 nM and 80 nM, respectiv