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

1 17beta-E(2) reduced the ROS levels and mitochondrial depolarization.

2 ting, NLRP3 stimulants caused SARM-dependent mitochondrial depolarization.

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

4 ed this free radical formation and prevented mitochondrial depolarization.

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

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

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

8 34 also normalized the hyperglycemia-induced mitochondrial depolarization.

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

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

11 accumulate on the mitochondria surface upon mitochondrial depolarization.

12 events after TR3 translocation but prior to mitochondrial depolarization.

13 idly and subsequently triggered a more rapid mitochondrial depolarization.

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

15 duced mitochondrial cytochrome c release and mitochondrial depolarization.

16 spondence to intracellular Ca+ increases and mitochondrial depolarization.

17 itochondria and greatly amplify NMDA-induced mitochondrial depolarization.

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

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

20 bility pathway responsible for the sustained mitochondrial depolarization.

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

22 ndicates that ROS are important mediators of mitochondrial depolarization.

23 triggered abrupt (and sometimes reversible) mitochondrial depolarization.

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

25 been observed in experiments under abnormal mitochondrial depolarization.

26 active oxygen species (ROS) that result from mitochondrial depolarization.

27 ut it did not prevent Ca(2+)-induced delayed mitochondrial depolarization.

28 mechanisms of Ca2+ alternans under abnormal mitochondrial depolarization.

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

30 tochondria elicit flickering-short pulses of mitochondrial depolarization.

31 gate the mechanisms of Ca2+ alternans during mitochondrial depolarization.

32 an increase in ROS levels and time-dependent mitochondrial depolarization.

33 ociates with mitochondria and contributes to mitochondrial depolarization.

34 ate mutase 5, at baseline and in response to mitochondrial depolarization.

35 mitochondrial shape changes that occur upon mitochondrial depolarization.

36 basal cell culture conditions and upon acute mitochondrial depolarization.

37 tinic acetylcholine receptor-dependent rapid mitochondrial depolarization.

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

39 to mitochondria and initiate mitophagy upon mitochondrial depolarization.

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

41 reactive oxygen species levels and inducing mitochondrial depolarization.

42 dependent target modification in response to mitochondrial depolarization.

43 was insensitive to inhibition of caspases or mitochondrial depolarization.

44 mitochondrial calcium clearance accelerated mitochondrial depolarization.

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

46 ulation contributed substantially to initial mitochondrial depolarizations.

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

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

49 Treatment with harmol induces a transient mitochondrial depolarization, a strong mitophagy respons

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

51 The results show that mitochondrial depolarization accompanies cytochrome c re

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

73 protected cells against beta-amyloid-induced mitochondrial depolarization and cell death.

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

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

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

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

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

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

80 receptor delta (PPARdelta) activity, causing mitochondrial depolarization and decreased oxidative pho

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

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

83 WHN-11 promoted mitochondrial depolarization and fission, suppressing th

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

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

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

87 Confocal microscopy revealed mitochondrial depolarization and inner membrane permeabi

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

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

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

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

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

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

94 the manifold nano-structural consequences of mitochondrial depolarization and provide a baseline for

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

96 Mitochondrial depolarization and reduced glutathione dep

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

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

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

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

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

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

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

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

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

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

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

108 nic channelrhodopsin, triggering cancer cell mitochondrial depolarization and subsequent cell death.

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

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

111 Interestingly, mitochondrial depolarization and subsequent necrosis can

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

113 bility transition pore (PTP), which leads to mitochondrial depolarization and swelling, the major sig

114 OGD withdrawal substantially attenuated the mitochondrial depolarization and the changes in synaptic

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

116 KCO-induced mitochondrial depolarization and transient KCa current a

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

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

119 , whose phosphorylation states increase upon mitochondrial depolarization and whose suppression inhib

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

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

122 d mitochondrial-triggered apoptosis profile, mitochondrial depolarization, and heightened oxidative s

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

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

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

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

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

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

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

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

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

132 Mitochondrial depolarization assays suggest that 4 acts

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

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

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

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

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

138 M1 allowed mitochondrial depolarization but blocked procaspase-9 pr

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

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

141 utely in the genesis of Ca2+ alternans after mitochondrial depolarization, but their roles can be sig

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

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

144 r MN-induced oxidative stress, but not after mitochondrial depolarization by carbonyl cyanide m-chlor

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

146 ur knowledge, show that optogenetic-mediated mitochondrial depolarization can be well controlled to d

147 We show that mitochondrial depolarization can cause Ca(2+) waves and

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

149 MT on key apoptosis signaling events such as mitochondrial depolarization, caspase activation, lysoso

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

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

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

153 Declining ATP levels after mitochondrial depolarization correlated with the absence

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

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

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

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

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

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

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

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

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

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

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

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

166 regulation of NCLX causes mtCa(2+) overload, mitochondrial depolarization, decreased expression of ce

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

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

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

170 Thus, SARM-dependent mitochondrial depolarization distinguishes NLRP3 activat

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

172 ved in DeltaPsi(m) instability, or sustained mitochondrial depolarization, during reperfusion by acut

173 delivery of genes to cancer cells to trigger mitochondrial depolarization, effectively inducing cell

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

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

176 This knockdown also reduced mitochondrial depolarization from exogenous Edelfosine o

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

178 he G2/M arrest was accompanied by apoptosis, mitochondrial depolarization, generation of reactive oxy

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

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

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

182 in prostaglandin E(2) (PGE(2)), which drives mitochondrial depolarization in CD8(+) T cells.

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

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

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

186 Concomitantly we observed mitochondrial depolarization in infected macrophages, an

187 tin E3 ligase pathways that are activated by mitochondrial depolarization in neurons.

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

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

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

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

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

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

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

195 KCO-induced mitochondrial depolarization increased the generation of

196 Mitochondrial depolarization induced Gp78-dependent expr

197 EIF2AK1 knockdown enhances mitochondrial depolarization-induced PINK1 stabilization

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

199 Mitochondrial depolarization inhibits ATP production, wh

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

201 d elevation in intracellular calcium levels, mitochondrial depolarization, intracellular trypsin acti

202 This suggests that mitochondrial depolarization is a consequence rather tha

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

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

205 uitin-dependent mitophagy pathway induced by mitochondrial depolarization is regulated by the mitocho

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

207 n kinase PTEN-induced kinase 1 (PINK1), upon mitochondrial depolarization, is an important intermedia

208 e to failure, intracellular calcium and ATP, mitochondrial depolarization, ischaemia-sensitive leak c

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

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

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

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

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

214 of FTY720 (both of which cause mild, ~ 10%, mitochondrial depolarization), markedly diminished the d

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

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

217 ession exacerbates, instead of ameliorating, mitochondrial depolarization-mediated cell death in HeLa

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

219 A slow mitochondrial depolarization observed before ouabain-SD

220 Mitochondrial depolarization occurred in many viable hep

221 We detected progressive mitochondrial depolarization occurring from ~2 h after i

222 en used the model to simulate the effects of mitochondrial depolarization on mitochondrial Ca(2+) cyc

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

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

225 he mitochondrial pathway, as demonstrated by mitochondrial depolarization, opening of mitochondrial t

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

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

228 ed by ATP production, which, when reduced by mitochondrial depolarization or ATP synthase inhibition,

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

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

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

232 Here, we use mitochondrial depolarization or the complex I inhibitor

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

234 not suppress mitochondrial motility, provoke mitochondrial depolarization, or dominantly suppress mit

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

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

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

238 We find that elevation of ROS in response to mitochondrial depolarization plays a critical role in pr

239 The onset of mitochondrial depolarization preceded changes in cell me

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

241 In conclusion, mitochondrial depolarization promotes Ca2+ alternans acu

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

243 In cells, mitochondrial depolarization reduces Rubicon:RAB7A coloc

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

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

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

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

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

249 Mechanistic assays confirmed mitochondrial depolarization, ROS generation, and inhibi

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

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

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

253 in enhanced mitochondrial shape changes upon mitochondrial depolarization, suggesting that ADA inhibi

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

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

256 Mitochondrial depolarization suppresses store-operated C

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

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

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

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

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

262 During mitochondrial depolarization, the post-tetanic potentiat

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

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

265 rease of intracellular ATP levels as well as mitochondrial depolarization together with a significant

266 mitochondria in axons, where GSDME promoted mitochondrial depolarization, trafficking defects, and n

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

268 Here, we demonstrate that mitochondrial depolarization triggers axon degeneration

269 The mitochondrial depolarization was also cyclosporin A-sens

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

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

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

273 Flavopiridol-induced mitochondrial depolarization was not blocked by caspase

274 Transient mitochondrial depolarization was observed 3-6 hours foll

275 Mitochondrial depolarization was prevented by calcium qu

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

277 The mitochondrial depolarization was sensitive to TTX and gl

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

279 Inner membrane permeabilization and mitochondrial depolarization were monitored by confocal

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

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

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

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

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

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

286 es to the outer mitochondrial membrane after mitochondrial depolarization with carbonyl cyanide m-chl

287 After mitochondrial depolarization with carbonyl cyanide m-chl

288 optogenetic-based technique for controllable mitochondrial depolarization with light.

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

290 mulation of pS65-Ub and mitophagic flux upon mitochondrial depolarization without USP30.

291 -2 homology domain 3 (BH3)-only proteins and mitochondrial depolarization, XIAP can permeabilize and