ライフサイエンスコーパス: mitoK(ATP)

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

2 5-hydroxydecanoate (5HD; 500 micromol/l), a mitoKATP channel blocker.

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

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

5 RRNYRRNY activated mitoK(ATP) channels via Cx43.

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

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

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

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

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

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

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

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

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

15 Steps between PKG and mitoKATP opening are unknown.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

30 34, opens surface K(ATP) channels but blocks mitoK(ATP) channels; the fact that this drug inhibits pr

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

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

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

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

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

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

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

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

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

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

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

42 Cardiac mitoKATP channel high-affinity (glyburide and glipizide)

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

72 the existence of a sulphonylurea-inhibitable mitoKATP channel.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

105 5HD and diazoxide as specific modulators of mitoK(ATP) channels in the heart.

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

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

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

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

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

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

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

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

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

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

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

117 -hydroxydecanoate is an effective blocker of mitoKATP channels.

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

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

120 risk during 1 to 90 days after initiation of mitoKATP channel high-affinity sulfonylureas (aHR, 6.06;

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

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

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

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

125 Use of mitoKATP channel high-affinity sulfonylureas vs low-affi

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

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

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

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

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

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

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

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

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

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

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

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

138 adenosine triphosphate-sensitive potassium (mitoKATP) channels have been speculated to account for t

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

155 1/2 values 45-75 microM) inhibited specific, mitoKATP-mediated K+ flux in both heart and liver mitoch

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

189 uggesting that high-affinity blockage of the mitoKATP channels could account for sulfonylurea-associa

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

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

192 Preconditioning protects the heart through mitoK(ATP).

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

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

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

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

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

198 that could be unequivocally associated with mitoKATP activity.