ライフサイエンスコーパス: mitochondrial depolarization

1 cell death in a process that was preceded by mitochondrial depolarization.

2 ed this free radical formation and prevented mitochondrial depolarization.

3 on and, in particular, calcium signaling and mitochondrial depolarization.

4 he Bak/Bax-dependent execution of UV-induced mitochondrial depolarization.

5 s and CaMKII play important roles in causing mitochondrial depolarization.

6 34 also normalized the hyperglycemia-induced mitochondrial depolarization.

7 ibited transient K(Ca) currents similarly to mitochondrial depolarization.

8 ed inhibition of transient K(Ca) currents by mitochondrial depolarization.

9 events after TR3 translocation but prior to mitochondrial depolarization.

10 idly and subsequently triggered a more rapid mitochondrial depolarization.

11 duced mitochondrial cytochrome c release and mitochondrial depolarization.

12 spondence to intracellular Ca+ increases and mitochondrial depolarization.

13 itochondria and greatly amplify NMDA-induced mitochondrial depolarization.

14 aspase activation, cytochrome c release, and mitochondrial depolarization.

15 e) but did not block cytochrome c release or mitochondrial depolarization.

16 bility pathway responsible for the sustained mitochondrial depolarization.

17 mitochondrial K(ATP) channel activation and mitochondrial depolarization.

18 ndicates that ROS are important mediators of mitochondrial depolarization.

19 triggered abrupt (and sometimes reversible) mitochondrial depolarization.

20 ted a spatial pattern similar to that of the mitochondrial depolarization.

21 tinic acetylcholine receptor-dependent rapid mitochondrial depolarization.

22 nyl cyanide m-chlorophenyl hydrazone-induced mitochondrial depolarization.

23 to mitochondria and initiate mitophagy upon mitochondrial depolarization.

24 s a factor in coupling matrix contraction to mitochondrial depolarization.

25 reactive oxygen species levels and inducing mitochondrial depolarization.

26 dependent target modification in response to mitochondrial depolarization.

27 was insensitive to inhibition of caspases or mitochondrial depolarization.

28 mitochondrial calcium clearance accelerated mitochondrial depolarization.

29 pearance of poly-ADP-ribose polymers and the mitochondrial depolarization.

30 17beta-E(2) reduced the ROS levels and mitochondrial depolarization.

31 ide, activated PINK1 in cells independent of mitochondrial depolarization.

32 eavage as a novel mechanism for GrB-mediated mitochondrial depolarization.

33 ulation contributed substantially to initial mitochondrial depolarizations.

34 ron transport chain blocker, induced a large mitochondrial depolarization (-84%, TMRM), reduced ROS,

35 entrations of chemical uncouplers to trigger mitochondrial depolarization, a stimulus that has been d

36 itophagy, leading to a downstream cascade of mitochondrial depolarization, aberrant calcium handling,

37 The results show that mitochondrial depolarization accompanies cytochrome c re

38 In conclusion, the MPT initiates mitochondrial depolarization after autophagic stimulatio

39 iphosphate production and were less prone to mitochondrial depolarization after chemotherapy, display

40 at interacts with VDAC, blocked and reversed mitochondrial depolarization after microtubule destabili

41 Prostaglandin E2 reduced apoptosis and mitochondrial depolarization after treatment with the Fa

42 e produced a block in glycolysis inhibition, mitochondrial depolarization, AIF translocation, and neu

43 in and DJ-1 pathways are strongly induced by mitochondrial depolarization, although a direct link bet

44 on or inhibition of respiration, all lead to mitochondrial depolarization, an increased Ca2+ influx t

45 cells treated with anti-hTfR IgG3-Av exhibit mitochondrial depolarization and activation of caspases

46 translocation of Bax to mitochondria causes mitochondrial depolarization and activation of caspases,

47 is the result of negative synergism between mitochondrial depolarization and altered organelle traff

48 re of calcium homeostasis that precedes both mitochondrial depolarization and an enhanced rate of pla

49 aspase-2 activation regulates PS-341-induced mitochondrial depolarization and apoptosis, suggesting t

50 ROS scavengers delay the progression of mitochondrial depolarization and apoptotic cell death.

51 phosphorylation of p70 S6 kinase but caused mitochondrial depolarization and ATP depletion within pr

52 vidence of a defect in the early response to mitochondrial depolarization and autophagosome formation

53 ccordingly, expression of catalase prevented mitochondrial depolarization and averted subsequent necr

54 hondria via the uniport transporter, causing mitochondrial depolarization and caspase 9 activation.

55 increase in mitochondrial mass and a lack of mitochondrial depolarization and caspase activation foll

56 induction of apoptosis by tamoxifen involves mitochondrial depolarization and caspase activation, and

57 oreceptors is mediated by calpain, involving mitochondrial depolarization and caspase-3 activation.

58 rocaspase-6 inhibited its activation despite mitochondrial depolarization and caspase-3 activation.

59 filomycin alone was not sufficient to induce mitochondrial depolarization and cell killing, but in th

60 ake and delayed PDT plus bafilomycin-induced mitochondrial depolarization and cell killing.

61 z-Leu-Leu-Tyr-CHN2 also delayed the onset of mitochondrial depolarization and cell necrosis during tr

62 els of the Apaf-1 and XIAP proteins, but not mitochondrial depolarization and cytochrome c release, a

63 al membrane remodeling, coupled with loss of mitochondrial depolarization and cytochrome c release, s

64 ntact cardiomyocytes, diazoxide also induced mitochondrial depolarization and decreased mitochondrial

65 phy 1 (OPA1) in fission deficiency prevented mitochondrial depolarization and decreased proton leak w

66 Apoptosis was accompanied by mitochondrial depolarization and elevation of caspase-3

67 ys were mediated by cyclophilin D and led to mitochondrial depolarization and fragmentation.

68 xicity has been attributed to the subsequent mitochondrial depolarization and generation of reactive

69 mary site of ROS production and demonstrated mitochondrial depolarization and increased mitochondrial

70 Confocal microscopy revealed mitochondrial depolarization and inner membrane permeabi

71 m 2 distinct pathways, one of which involves mitochondrial depolarization and is mediated by TMEM16F.

72 ndrial fragmentation and turnover rescue the mitochondrial depolarization and neurodegenerative pheno

73 JNK by RNS was density dependent and caused mitochondrial depolarization and nuclear condensation.

74 This effect is attributed to prevention of mitochondrial depolarization and of subsequent release o

75 an LC3-interaction region (LIR) domain upon mitochondrial depolarization and proteasome-dependent ou

76 with an NO donor induces a modest, sustained mitochondrial depolarization and protects cardiomyocytes

77 Nix promoted CCCP-induced mitochondrial depolarization and reactive oxygen species

78 Mitochondrial depolarization and reduced glutathione dep

79 f caspase-8, Bid, and Bax; and 3) subsequent mitochondrial depolarization and release of apoptosis-in

80 , caspase activation (caspases 3, 8, and 9), mitochondrial depolarization and release of cytochrome c

81 Both cell types displayed mitochondrial depolarization and release of cytochrome c

82 It caused a pronounced mitochondrial depolarization and release of cytochrome c

83 ines underwent apoptosis and associated with mitochondrial depolarization and relocalization of apopt

84 on of JNK or overexpression of ARC prevented mitochondrial depolarization and rescued H9c2 cells from

85 ondrial Ca(2+), resulting in lower levels of mitochondrial depolarization and resistance to excitotox

86 prevented the hypoxia-reoxygenation-induced mitochondrial depolarization and resulted in an enhancem

87 xanthine inhibited the peroxynitrite-induced mitochondrial depolarization and secondary superoxide pr

88 nfolded protein response was correlated with mitochondrial depolarization and secretion of interleuki

89 nhanced hydroperoxide generation, leading to mitochondrial depolarization and subsequent cell death.

90 Both CI-1010-induced mitochondrial depolarization and subsequent increases in

91 of the N-terminal Hax-1 fragment results in mitochondrial depolarization and subsequent lysosomal de

92 Interestingly, mitochondrial depolarization and subsequent necrosis can

93 resent two independent pathways that control mitochondrial depolarization and subsequent necrosis of

94 molecule Bad resulting in the inhibition of mitochondrial depolarization and the release of cytochro

95 KCO-induced mitochondrial depolarization and transient KCa current a

96 apoptosis involved caspase-3 activation and mitochondrial depolarization and was dependent on gp41 f

97 agonists convulxin/thrombin fully relied on mitochondrial depolarization and was virtually absent in

98 ogram characterized by cytochrome c release, mitochondrial depolarization, and caspase activation.

99 ase activation, phosphatidylserine exposure, mitochondrial depolarization, and DNA fragmentation were

100 uced a larger increase in cytosolic calcium, mitochondrial depolarization, and necro-apoptotic cell d

101 of ddC-induced "neuritic pruning," neuronal mitochondrial depolarization, and neuronal necrotic deat

102 y, we assessed Treg cell induction in vitro, mitochondrial depolarization, and recruitment of PTEN to

103 -induced apoptosis including cell shrinkage, mitochondrial depolarization, annexin binding, caspase a

104 can yield increased production of ceramide, mitochondrial depolarization, apoptosis, and cell death.

105 fect is accompanied by proliferation arrest, mitochondrial depolarization, apoptosis, and immune clea

106 nking also protects against arsenite-induced mitochondrial depolarization as well as caspase-9 cleava

107 ntry through Ca-A/K channels triggered rapid mitochondrial depolarization, as assessed by using the p

108 for 90 minutes caused a modest but sustained mitochondrial depolarization, as judged by JC-1 fluoresc

109 Mitochondrial depolarization assays suggest that 4 acts

110 ef exposure to either AMPA or kainate caused mitochondrial depolarization, assessed using tetramethyl

111 stably transfected cells was associated with mitochondrial depolarization, Bax activation, cytochrome

112 de drives ROS generation by inducing a small mitochondrial depolarization, because nanomolar CCCP, a

113 d that TNFalpha induced onset of the MPT and mitochondrial depolarization beginning 9 h after TNFalph

114 not only prevents cell death from excessive mitochondrial depolarization but also activates AMPK sig

115 M1 allowed mitochondrial depolarization but blocked procaspase-9 pr

116 s treated with Vpr are highly susceptible to mitochondrial depolarization, but develop resistance fol

117 uction in cultured mammalian cells following mitochondrial depolarization, but its role in vivo is no

118 ochondrial permeability transition (MPT) and mitochondrial depolarization by 2-3 h after anti-Fas ant

119 The extent of mitochondrial depolarization by a BIM BH3 peptide in vit

120 report that in neurons, unlike other cells, mitochondrial depolarization by carbonyl cyanide m-chlor

121 imulation of oxygen consumption, followed by mitochondrial depolarization, caspase activation, and ph

122 tial in astrocytes, accompanied by transient mitochondrial depolarizations caused by reversible openi

123 Hepatic mitochondrial depolarization, cell death, and MPT were d

124 s also manifested a considerable increase in mitochondrial depolarization correlated with increased g

125 Declining ATP levels after mitochondrial depolarization correlated with the absence

126 Our data suggest that astrocyte mitochondrial depolarization could be a previously unrec

127 a(2+) sparks and transient K(Ca) currents by mitochondrial depolarization could not be explained by a

128 lpha, blockade of MPT pore opening prevented mitochondrial depolarization, cytochrome c redistributio

129 mitochondrial-dependent apoptosis, including mitochondrial depolarization, cytochrome C release and t

130 chondrial changes consistent with apoptosis (mitochondrial depolarization, cytochrome c release), DNA

131 of liver cells to saturated FFAs resulted in mitochondrial depolarization, cytochrome c release, and

132 JA6017-inhibitable manner with bid cleavage, mitochondrial depolarization, cytochrome c release, and

133 apoptosis (phosphatidylserine translocation, mitochondrial depolarization, cytochrome c release, and

134 olI but not Fn inhibited doxorubicin-induced mitochondrial depolarization, cytochrome c release, and

135 ssion inhibited mitochondrial fragmentation, mitochondrial depolarization, cytochrome c release, reac

136 nide m-chlorophenyl hydrazone (CCCP)-induced mitochondrial depolarization decreased mitochondrial mas

137 eability transition (MPT) pore, resulting in mitochondrial depolarization, decreased ATP synthesis, a

138 ndices within whole cells (active caspase-3, mitochondrial depolarization [DeltaPsim] and TUNEL).

139 Overexpression of ARC, although preventing mitochondrial depolarization, did not affect either JNK

140 cell viability, organelle damage manifest by mitochondrial depolarization, disordered autophagy, and

141 hibit glucocorticoid-induced cell shrinkage, mitochondrial depolarization, DNA fragmentation, and cel

142 In voltage-clamped (-40 mV) cells, mitochondrial depolarization elevated global [Ca(2+)](i)

143 rmeability transition but not so severe that mitochondrial depolarization exceeds threshold.

144 This knockdown also reduced mitochondrial depolarization from exogenous Edelfosine o

145 ease from liver mitochondria or GCDC-induced mitochondrial depolarization from isolated hepatocytes,

146 The compounds caused apoptosis of the cells, mitochondrial depolarization, generation of reactive oxy

147 a dominant negative form of Hax-1, mediating mitochondrial depolarization in a cyclophilin D-dependen

148 GzmB still induces mitochondrial depolarization in Bax, Bak double knockout

149 d MPT in isolated mitochondria and prevented mitochondrial depolarization in cells treated with 3NP.

150 on microscope to examine the effect of local mitochondrial depolarization in guinea pig ventricular m

151 ive and glycolytic respiration together with mitochondrial depolarization in human and mouse white ad

152 Concomitantly we observed mitochondrial depolarization in infected macrophages, an

153 f acetylcholine, which now also causes rapid mitochondrial depolarization in neurons.

154 ed mitochondrial trafficking correlated with mitochondrial depolarization in palmitate-treated DRG ne

155 profiling, a functional assay that assesses mitochondrial depolarization in response to BH3-only pep

156 the onset of rigor and increased the rate of mitochondrial depolarization in response to CN-_DOG.

157 There was also decreased mitochondrial depolarization in response to TNF-alpha +

158 l hyperpolarization in the COLO 16 cells and mitochondrial depolarization in the rho(0) clones.

159 nner membrane anion channel causes transient mitochondrial depolarizations in a single mitochondrion

160 KCO-induced mitochondrial depolarization increased the generation of

161 Mitochondrial depolarization induced Gp78-dependent expr

162 ts suggest that palmitate induces DRG neuron mitochondrial depolarization, inhibiting axonal mitochon

163 Data also suggest that mitochondrial depolarization inhibits Ca(2+) sparks and

164 This suggests that mitochondrial depolarization is a consequence rather tha

165 the UV sensitivity of cells, and the ensuing mitochondrial depolarization is entirely abrogated by Bi

166 We have shown that Vpr-induced mitochondrial depolarization is mediated by TNFR-associa

167 A global phase transition (mitochondrial depolarization) is shown to occur when a c

168 ABT-737 plus L-asparaginase induced greater mitochondrial depolarization (JC-1 staining); mitochondr

169 It has been shown that transient single mitochondrial depolarizations, known as flickers, tend t

170 ating this pathway, and that small and large mitochondrial depolarizations lead to differential regul

171 These results indicate that mitochondrial depolarization leads to a voltage-independ

172 yryl-cAMP (DB), coupled with measurements of mitochondrial depolarization, lipolysis, kinase activiti

173 nd permeability transition pore-independent (mitochondrial depolarization) mechanisms.

174 KA) activity, whereas Opa1 cleavage required mitochondrial depolarization mediated by FFAs released a

175 ce cell necrosis, significant ATP depletion, mitochondrial depolarization nor the MMPT.

176 A slow mitochondrial depolarization observed before ouabain-SD

177 Mitochondrial depolarization occurred in many viable hep

178 posure, and the effects of cyclosporin A and mitochondrial depolarization on presynaptic resting calc

179 llowing neurons to maintain ATP levels after mitochondrial depolarization only modestly increased Par

180 rgeted the mitochondrial matrix resulting in mitochondrial depolarization, opening of the permeabilit

181 cells infected with MCF13 MLV did not reveal mitochondrial depolarization or a significant change in

182 o, we pre-activated XIAP at mitochondria via mitochondrial depolarization or by artificially targetin

183 ndria with similar kinetics following either mitochondrial depolarization or localized generation of

184 sitive and specific indicator of significant mitochondrial depolarization or recovery during I-R.

185 ngaged defences that induced transient, mild mitochondrial depolarization or uncoupling.

186 e the mechanism governing such resistance to mitochondrial depolarization, our results show that prio

187 gents synergistically induced ATP depletion, mitochondrial depolarization, oxidative stress, and necr

188 ibroblast (MEF) cells, Casp8p41 causes rapid mitochondrial depolarization (P < 0.001), yet Casp8p41 e

189 The onset of mitochondrial depolarization preceded changes in cell me

190 oglial mitochondrial respiration, leading to mitochondrial depolarization, production of free radical

191 calmodulin-regulated kinase II (CaMKII), and mitochondrial depolarization reduced impact-induced chon

192 the parasite Leishmania donovani (Ld) causes mitochondrial depolarization, reduces mitochondrial dyna

193 lin, an adenylate cyclase activator, induces mitochondrial depolarization, release of cytochrome c in

194 thyl ester to visualize onset of the MPT and mitochondrial depolarization, respectively.

195 d mitochondrial ROS production and prevented mitochondrial depolarization, respiratory impairment, an

196 cells utilizing usual glycolytic metabolism, mitochondrial depolarization robustly triggered Parkin-m

197 entiated into dopaminergic neurons that upon mitochondrial depolarization showed impaired recruitment

198 tivation of p38 and TR3 expression, prior to mitochondrial depolarization, subsequent release of cyto

199 h adenosine triphosphate (ATP) depletion and mitochondrial depolarization suggesting that ceramides c

200 +, were associated with propagating waves of mitochondrial depolarization, suggesting that propagatin

201 cytochrome c release, it was unable to block mitochondrial depolarization, suggesting that these are

202 Mitochondrial depolarization suppresses store-operated C

203 Ca(2+) and/or Pb(2+) induced mitochondrial depolarization, swelling, and cytochrome c

204 d with cortical mitochondria, as measured by mitochondrial depolarization, swelling, Ca2+ uptake, rea

205 tor involved in determining the threshold of mitochondrial depolarization that leads to the productio

206 KA exposure induced a partial mitochondrial depolarization that was enhanced by oligom

207 complex I and F(0)F(1)-ATP synthase induced mitochondrial depolarization that was independent of the

208 During mitochondrial depolarization, the post-tetanic potentiat

209 Thus, c-IAP-2 may prevent Vpr-mediated mitochondrial depolarization through stabilizing TRAF-1/

210 d with apoptosis revealed that HSH2 inhibits mitochondrial depolarization to a significant degree, wh

211 The results demonstrate that regional mitochondrial depolarization triggered by oxidative stre

212 Here, we demonstrate that mitochondrial depolarization triggers axon degeneration

213 The mitochondrial depolarization was also cyclosporin A-sens

214 PS-341-induced mitochondrial depolarization was attenuated by Z-VDVAD-F

215 Weight change was measured, and mitochondrial depolarization was determined using JC-1 s

216 Barbiturate-induced mitochondrial depolarization was increased by the ATP sy

217 Flavopiridol-induced mitochondrial depolarization was not blocked by caspase

218 Transient mitochondrial depolarization was observed 3-6 hours foll

219 Mitochondrial depolarization was prevented by calcium qu

220 hronous release evoked by stimulation during mitochondrial depolarization was produced by the elevati

221 The mitochondrial depolarization was sensitive to TTX and gl

222 the other hand, many studies have shown that mitochondrial depolarization waves and whole-cell oscill

223 Inner membrane permeabilization and mitochondrial depolarization were monitored by confocal

224 These effects of mitochondrial depolarization were not accompanied by a s

225 The first order rate constants for mitochondrial depolarization were: C6, k=0.31+/-0.02 min

226 a 3-fold increase in apoptotic activity and mitochondrial depolarization when compared with vector t

227 sufficient to evoke cytochrome c release and mitochondrial depolarization, whereas full-length Bid wa

228 ate that Casp8p41 requires Bax/Bak to induce mitochondrial depolarization, which leads to caspase 9 a

229 release increased [Ca(2+)](mito) and induced mitochondrial depolarization, which stimulated mitochond

230 After mitochondrial depolarization with carbonyl cyanide m-chl

231 UCD38B in human glioma cells corresponds to mitochondrial depolarization with the release and nuclea

232 -2 homology domain 3 (BH3)-only proteins and mitochondrial depolarization, XIAP can permeabilize and