ライフサイエンスコーパス: cytochrome c release

1 spases activation, Bcl-xL sequestration, and cytochrome c release.

2 disrupts Bcl-2/Bid interaction, and induces cytochrome c release.

3 ic interference with cristae remodelling and cytochrome c release.

4 Puma-induced apoptosis, acting downstream of cytochrome c release.

5 t compromised energy supply and proapoptotic cytochrome c release.

6 athogenic parkin mutants failed to influence cytochrome c release.

7 els of parkin were inversely correlated with cytochrome c release.

8 he presence of FasL to enhance mitochondrial cytochrome c release.

9 etion activates C2 upstream of mitochondrial cytochrome c release.

10 binding per se was not sufficient to inhibit cytochrome c release.

11 inhibition of iPLA(2)beta or NSMase prevents cytochrome c release.

12 cells by restoring caspase-3 activation and cytochrome c release.

13 tBid is targeted to mitochondria and causes cytochrome c release.

14 ocalization to mitochondria and induction of cytochrome c release.

15 ptosis by promoting caspase-3 activation and cytochrome c release.

16 n, permeability transition pore opening, and cytochrome c release.

17 d can induce its oligomerization, leading to cytochrome c release.

18 uired only for events that are downstream of cytochrome c release.

19 both Drp1 binding to Mff and stress-induced cytochrome c release.

20 ial permeability transition pore opening and cytochrome c release.

21 XIAP occurs independently of Drp1-regulated cytochrome c release.

22 initiate apoptosis upstream of mitochondrial cytochrome c release.

23 in HDMEC-Bcl-2 cells was not associated with cytochrome c release.

24 ion, internucleosomal DNA fragmentation, and cytochrome c release.

25 Readdition of NGF also immediately inhibits cytochrome c release.

26 tin incubation, including Bax activation and cytochrome c release.

27 e-8 activation and proximal to mitochondrial cytochrome c release.

28 t not a noncleavable mutant (D59E), restored cytochrome c release.

29 of the mitochondrial membrane potential and cytochrome C release.

30 rotective Bcl-2 family protein, resulting in cytochrome c release.

31 en species (ROS), and initiate apoptosis via cytochrome c release.

32 ation that binds the active Bax and inhibits cytochrome c release.

33 osolic conformational state, which prevented cytochrome c release.

34 1 prevented hyperoxia-induced cell death and cytochrome c release.

35 activity were observed rapidly following the cytochrome c release.

36 , disrupted Ca(2+) homeostasis, and enhanced cytochrome c release.

37 effects of rat v2 and human v4 by modulating cytochrome c release.

38 swelling and depolarization, and accelerated cytochrome c release.

39 tin-treated cells, which was associated with cytochrome c release.

40 mitochondria and promotes fragmentation and cytochrome c release.

41 n the mitochondrial translocation of Bax and cytochrome C release.

42 hat measure Bax subcellular localization and cytochrome c release.

43 ndrial translocation of BAX and BAX-mediated cytochrome c release.

44 ondria treated with beta-GA showed increased cytochrome c release.

45 n very low doses lead eventually to complete cytochrome c release.

46 caspase-3, poly-(ADP-ribose) polymerase, and cytochrome c release.

47 not lead to cerebral caspase-3 activation or cytochrome-c release.

48 tent of cells was observed immediately after cytochrome c release 6 h after apoptosis induction and t

49 ase, induction of VDAC1 oligomerization, and cytochrome c release, a sequence of events leading to ap

50 thelial cell cytoprotection independently of cytochrome c release: (a) increased survivin expression,

51 that results in its mitochondria targeting, cytochrome c release, activation of caspase-9, and apopt

52 ormational changes, Bax/Bak oligomerization, cytochrome c release, activation of caspases, and poly(A

53 rial outer membrane permeabilization (MOMP), cytochrome c release, activation of caspases-3 and -9, a

54 epolarization (JC-1 staining); mitochondrial cytochrome c release; activation of Bax, Bid, and caspas

55 increased caspase-9 activation and increased cytochrome c release after Jo-2 exposure.

56 antiapoptotic Bcl-2 proteins, which inhibit cytochrome c release, also display pore activity in mode

57 ts of apoptosis, namely Bax accumulation and cytochrome c release, also were ameliorated.

58 respiration, and ATP production and induced cytochrome c release, although the lack or inactivation

59 null cells exhibiting delayed mitochondrial cytochrome c release and activation of caspase-3.

60 vation of caspase-7, which is independent of cytochrome c release and activation of caspase-9 and cas

61 activation of JNK1/2, leading ultimately to cytochrome c release and activation of caspases.

62 e mitochondrial outer membrane, resulting in cytochrome c release and activation of effector caspases

63 ss of mitochondrial transmembrane potential, cytochrome c release and activation of terminal caspases

64 uated apoptosis as measured by mitochondrial cytochrome c release and activation of the caspase casca

65 ene (SCO2), which is critical for preventing cytochrome c release and activation of the intrinsic apo

66 S) scavengers suppressed the coordination of cytochrome c release and also inhibited Bid-induced cell

67 Importantly, this induced interaction caused cytochrome c release and apoptosis and was directly inhi

68 sembly-resistant mutant Opa1 (Q297V) blocked cytochrome c release and apoptosis but not Bax activatio

69 investigated the regulation of tBid-induced cytochrome c release and apoptosis by phospholipid scram

70 The latter leads to cytochrome c release and apoptosis in human lung cancer

71 parkin on mitochondrial mechanisms governing cytochrome c release and apoptosis, which may be relevan

72 hondrial fragmentation was observed prior to cytochrome c release and apoptosis.

73 role in the execution of DNA damage-induced cytochrome c release and apoptosis.

74 Bid interaction at mitochondria, suppressing cytochrome c release and apoptosis.

75 anied by the amelioration of Bax activation, cytochrome c release and apoptosis.

76 onally converts it to a killer that triggers cytochrome c release and apoptosis.

77 logical inhibition of GSK-3, which prevented cytochrome c release and apoptosis.

78 es and formation of Bax oligomers leading to cytochrome c release and apoptosis.

79 chondrial outer membrane (MOM), which causes cytochrome c release and apoptosis.

80 plays an important role in Bax/Bak-mediated cytochrome c release and apoptosis.

81 death involved effector caspase activation, cytochrome c release and Bax oligomerization in the mito

82 ote cell viability by impeding mitochondrial cytochrome c release and by inhibiting subsequent caspas

83 photoreceptor synapse was demonstrated with cytochrome c release and caspase 3 activation within the

84 se 8 activation and downstream mitochondrial cytochrome c release and caspase 3 and caspase 7 activat

85 ed cells treated with staurosporine did have cytochrome c release and caspase 9 activation, indicatin

86 ced downstream markers of caspase-dependent (cytochrome c release and caspase activation) and caspase

87 late mitochondrial outer membrane integrity, cytochrome c release and caspase activation.

88 These pathways regulate late cytochrome c release and caspase-3 activation.

89 h decreased Akt phosphorylation, increase in cytochrome c release and caspase-3 cleavage, as well as

90 the mitochondrial pathway of apoptosis with cytochrome c release and caspase-3 cleavage.

91 induced endothelial cell death by inhibiting cytochrome c release and caspase-9/3 activation.

92 SUMOylation, which suppresses Drp1-mediated cytochrome c release and caspase-mediated cell death.

93 , altering the Mcl-1/Bak ratio, facilitating cytochrome c release and cell death.

94 n cell survival/cell death through regulated cytochrome c release and control of apoptosis, we sought

95 les of nuclear p53 activation, mitochondrial cytochrome c release and cytosolic caspase activation th

96 hermore, TRPC1 overexpression also inhibited cytochrome c release and decreased BAX protein levels re

97 ria by autophagy, thereby reducing cytosolic cytochrome c release and downstream caspase activation a

98 ion, caspase-3 and caspase-9 activation, and cytochrome c release and increased Bcl-2 levels.

99 igands capable of inducing effector-mediated cytochrome c release and liposome permeabilization, even

100 In turn, O(2)(*-) facilitates cytochrome c release and mitochondrial membrane potentia

101 in a feedback amplification loop to promote cytochrome c release and other mitochondrial events in a

102 by DNA fragmentation, caspase-3/7 activity, cytochrome c release and over 24 h was accompanied by su

103 PS-341-induced cytochrome c release and phosphatidylserine externalizat

104 isintegrates during apoptosis at the time of cytochrome c release and prior to caspase activation, yi

105 sis, including mitochondrial depolarization, cytochrome C release and the activation of specific casp

106 eling [TUNEL]), mitochondrial death pathway (cytochrome c release), and endoplasmic reticulum (ER) st

107 ubicin-induced mitochondrial depolarization, cytochrome c release, and activation of caspase-9 and -3

108 on, increased mitochondrial Bax/Bcl-2 ratio, cytochrome c release, and activation of caspases-9 and c

109 cation of BAX to the mitochondrial membrane, cytochrome c release, and activation of downstream apopt

110 en consumption, extracellular acidification, cytochrome c release, and apoptosis in retinal endotheli

111 TRAIL-mediated mitochondrial potential loss, cytochrome c release, and apoptosis, suggesting specific

112 uppressed albumin-induced Bax translocation, cytochrome c release, and apoptosis.

113 e oxygen species generation, Bax activation, cytochrome C release, and apoptosis.

114 at) is sufficient to trigger Bax activation, cytochrome c release, and apoptosis.

115 triphosphate (ATP) depletion, mitochondrial cytochrome c release, and caspase activation.

116 Decreases of hepatic ATP, mitochondrial cytochrome c release, and caspase-3 activation after MHX

117 potential collapse, chromosome condensation, cytochrome C release, and caspase-3 activation induced b

118 translocation, mitochondrial depolarization, cytochrome c release, and caspase-3 activation) was seve

119 mulating reactive oxygen species production, cytochrome c release, and caspase-9 activation.

120 on, liposome permeabilization, mitochondrial cytochrome c release, and cell death.

121 ine (CSA) reduced LKT-mediated cytotoxicity, cytochrome c release, and collapse of the psi(m).

122 Mitochondrial swelling, cytochrome c release, and decreases in both mitochondria

123 idative stress biomarker aconitase activity, cytochrome c release, and expression of oxidative stress

124 e permeability, mitochondrial damage without cytochrome c release, and extensive cytoplasmic vacuolat

125 As resulted in mitochondrial depolarization, cytochrome c release, and increased ROS production.

126 lower levels of heat-induced Bak activation, cytochrome c release, and loss of mitochondrial membrane

127 cal for Bid-induced OMM permeabilization and cytochrome c release, and Mfn1/2(-/-) cells show dysregu

128 ssociated with an absence of Bak activation, cytochrome c release, and mitochondrial membrane depolar

129 LDH release assay, cytochrome c release, and mitochondrial membrane potenti

130 reased association of Bax with mitochondria, cytochrome c release, and neuronal apoptosis.

131 o the MOM bypasses the need for Mff to evoke cytochrome c release, and occludes the effect of SENP3 o

132 roglial/macrophage and astrocyte activation, cytochrome c release, and oxidative DNA damage.

133 uperoxide generation, active RhoA abundance, cytochrome c release, and p47phox expression and suppres

134 disappearance of intact 21-kDa Bid protein, cytochrome c release, and predominant procaspase-3 cleav

135 al burden, preserve ATP generation, decrease cytochrome c release, and prevent caspase-9 activation,

136 to altered mitochondrial membrane potential, cytochrome c release, and reactive oxygen species releas

137 or cells, ABT-263 induces Bax translocation, cytochrome c release, and subsequent apoptosis.

138 , an increase in mitochondrial permeability, cytochrome c release, and the activation of caspase-9.

139 ation of Nampt increased caspase 3 cleavage, cytochrome c release, and TUNEL-positive cells, which we

140 ate that iPLA(2)beta modulates mitochondrial cytochrome c release, and we find that thapsigargin and

141 hondrial membrane potential, ATP levels, and cytochrome c release, and with a TUNEL assay.

142 d calcium tolerance, decreased mitochondrial cytochrome C release,and enhance phosphorylation of mito

143 loss of mitochondrial membrane potential and cytochrome c release; and (iv) activation of initiator c

144 p53 expression, cytochrome c release, apoptosome formation, and caspase-

145 mitochondrial membrane permeabilization and cytochrome c release are central to apoptosis.

146 Pin1-/- mice: oligodendrocyte apoptosis and cytochrome c release are reduced in JNK3-/- but elevated

147 rn blot analysis showed a marked decrease in cytochrome c release as a result of SAC treatment.

148 The MitoCapture mitochondrial apoptosis and cytochrome c release assays indicated that t-Darpp expre

149 ed from RRECs were treated with beta-GA, and cytochrome c release assessed by Western blot.

150 =5 microM rapidly (i.e., within 4 h) induced cytochrome c release, Bax mitochondrial translocation, a

151 7 and mitochondrial translocation of Bax and cytochrome c release but not c-Jun N-terminal kinase act

152 c BH3-only proteins Bid and Bim induced full cytochrome c release but only a subtle alteration of cri

153 tage-thresholds of mPT opening inferred from cytochrome c release, but intact cells showed no differe

154 ental changes in the threshold for apoptotic cytochrome c release, but the substrate(s) involved in p

155 ed Bcl-2-like protein, F1L, which suppresses cytochrome c release by binding Bcl-2 family proteins, i

156 Activated after injury, JNK3 induces cytochrome c release by facilitating the degradation of

157 ppresses apoptosis upstream of mitochondrial cytochrome c release by phosphorylating caspase-2 within

158 acidification using an XF-24 flux analyzer, cytochrome c release by Western blot, and apoptosis by t

159 y protecting the mitochondria and preventing cytochrome c release, by activating cell survival pathwa

160 ome c release, resulting in reduced cellular cytochrome c release capacity.

161 l membrane potential and platelet apoptosis (cytochrome c release, caspase 3 activation, and phosphat

162 xation, and attenuated apoptosis by limiting cytochrome c release, caspase 3 activity, and cleavage o

163 bserved in mitochondrial membrane potential, cytochrome c release, caspase 9 activation, or ratios of

164 Drp1 attenuated mitochondrial fragmentation, cytochrome c release, caspase activation, and apoptosis.

165 is inducible, reversible, and independent of cytochrome c release, caspase activation, and DNA fragme

166 or ER-directed Nix mutants exhibited similar cytochrome c release, caspase activation, annexin V and

167 nide-induced mitochondrial permeabilization, cytochrome c release, caspase and PARP cleavage, consist

168 ase (JNK) activation, Bcl-2 phosphorylation, cytochrome c release, caspase-3 activation and DNA fragm

169 Knockdown of either protein reduced cytochrome c release, caspase-3 activation, and apoptosi

170 gated Ang II-induced apoptosis by inhibiting cytochrome c release, caspase-3 activation, and DNA frag

171 ting IRF8 function resulted in inhibition of cytochrome c release, caspase-9 and caspase-3 activation

172 that a death signal generated downstream of cytochrome c release diffused to neighboring cells and u

173 been proposed that Bax-like proteins induce cytochrome c release during apoptosis via pore formation

174 ter ADP-phosphorylating activity and reduced cytochrome C release during reperfusion.

175 ptosis and that tBid may function to promote cytochrome c release during this process as part of a fe

176 he mitochondrial permeability transition and cytochrome c release, followed by caspase-3 activation,

177 Indeed, Bid cleavage and cytochrome c release following 15d-PGJ(2) but not MEHP t

178 mitochondria to elevated Ca2+ and diminishes cytochrome c release from brain mitochondria by antagoni

179 Pancaspase inhibitors did not prevent cytochrome c release from cells expressing mu1, indicati

180 In support of these findings, cytochrome c release from iPLA(2)gamma(-/-) mitochondria

181 dditionally, recombinant p73 protein induced cytochrome c release from isolated mitochondria providin

182 ompromised in mediating OMMP, as measured by cytochrome c release from isolated mitochondria.

183 o bind p53 and potently inhibits p53-induced cytochrome c release from isolated mitochondria.

184 noma cell lines from apoptosis by inhibiting cytochrome c release from mitochondria after treatment w

185 ppressed 4HPR-induced c-Jun phosphorylation, cytochrome c release from mitochondria and apoptosis.

186 production, which prevented Ca(2+)-mediated cytochrome c release from mitochondria and decreased rea

187 mitochondrial membrane potential, it delays cytochrome c release from mitochondria and further progr

188 of CypD respectively decreases or increases cytochrome c release from mitochondria and overall cell

189 lium to ketamine resulted in apoptosis, with cytochrome c release from mitochondria and significant s

190 Moreover, cytochrome c release from mitochondria and subsequent ap

191 s confirm that CypD has a limiting effect on cytochrome c release from mitochondria and that such an

192 ty was directly related to the inhibition of cytochrome c release from mitochondria and the activity

193 ession of c-Myc and caspase-2 is crucial for cytochrome c release from mitochondria during cytotoxic

194 Caspase-2 promoted cytochrome c release from mitochondria in the presence o

195 D as a Bcl2 collaborator and an inhibitor of cytochrome c release from mitochondria independent of th

196 itochondrion-mediated apoptosis, as shown by cytochrome c release from mitochondria to cytoplasm, act

197 1-deleted hFis1, and significantly decreased cytochrome c release from mitochondria upon apoptotic in

198 f the intrinsic cell death pathway; however, cytochrome c release from mitochondria was diminished in

199 EL-positive cells, caspase-3 activation, and cytochrome c release from mitochondria was observed in t

200 against the accumulation and toxicity (i.e. cytochrome c release from mitochondria) of intracellular

201 tent (alpha/beta + alpha)-peptide can induce cytochrome C release from mitochondria, an early step in

202 ction decreases GzmB-induced Bax activation, cytochrome c release from mitochondria, and subsequent e

203 apoptotic signaling, evidenced by increased cytochrome C release from mitochondria, caspase 3 activi

204 tein-protein interactions is associated with cytochrome c release from mitochondria, caspase-3 activa

205 Many proapoptotic stimuli trigger cytochrome c release from mitochondria, promoting the fo

206 interacts transiently with Bax and promotes cytochrome c release from mitochondria.

207 olves p53 activation, bax transcription, and cytochrome c release from mitochondria.

208 a drug library to identify new inhibitors of cytochrome c release from mitochondria.

209 ation from the cytoplasm to mitochondria and cytochrome c release from mitochondria.

210 potent antiapoptotic protein, which prevents cytochrome c release from mitochondria.

211 ently blocks Bid-activated Bax/Bak-dependent cytochrome c release from mitochondria.

212 tes its antiapoptotic function by regulating cytochrome c release from mitochondria.

213 trinsic apoptosis inducer, c-FLIP suppressed cytochrome c release from mitochondria.

214 caspase-3 that was associated with increased cytochrome c release from mitochondria.

215 Bax interaction, oligomerization of Bak, and cytochrome c release from mitochondria.

216 hondrial dysfunction, Bax translocation, and cytochrome c release from mitochondria.

217 cells, cleaved PARP, cleaved caspase-3, and cytochrome c release from mitochondria.

218 Rifampicin also inhibited cytochrome c release from the mitochondria and caspase 3

219 evels, increase ROS accumulation, facilitate cytochrome c release from the mitochondria to the cytoso

220 showed an induction of Bax translocation and cytochrome c release from the mitochondria to the cytoso

221 r membrane permeabilization characterized by cytochrome c release from the mitochondrial intermembran

222 nduced Bax translocation to mitochondria and cytochrome c release from the organelles, further confir

223 by the ability of the BH3 mimetic to induce cytochrome c release from their isolated mitochondria.

224 Third, cytochrome c, released from mitochondria early in apopto

225 However, the specific biologic importance of cytochrome c release has not been demonstrated in Huntin

226 ional BH3-like domain, which is required for cytochrome c release in cells and isolated mitochondria

227 rrently with mitochondrial fragmentation and cytochrome c release in CGNs deprived of depolarizing po

228 nuclear translocation of AIF, and attenuated cytochrome c release in cytosol.

229 support for the important functional role of cytochrome c release in HD.

230 Finally, MitoBloCK-6 induced apoptosis via cytochrome c release in human embryonic stem cells (hESC

231 ly (Bax, Bid, and Bim) are unable to trigger cytochrome c release in MK-STYX-depleted cells, placing

232 tic insults is associated with inhibition of cytochrome c release in most but not all neurons, indica

233 We found Bax activation and cytochrome c release in neurons following infection of n

234 h increased Bax to Bcl-2 ratios and elevated cytochrome c release in the LV sections of DOX-treated C

235 ability pore transition (MPT) and consequent cytochrome c release in these cells.

236 th mitochondrial membrane depolarization and cytochrome c release indicating activation of the mitoch

237 reactive oxygen species (ROS) production and cytochrome c release, indicating that lumican-induced di

238 ther confirmed by mitochondrial swelling and cytochrome c release induced by Ca(2+) overload.

239 In isolated mitochondria, Nutlin-3 inhibited cytochrome c release induced by Ca2+, Bim peptide, and r

240 myocyte mitochondrial membrane potential and cytochrome c release induced by tumor necrosis factor-al

241 en correlated with blockade of mitochondrial cytochrome c release, inhibition of Bax and Bak activati

242 DNA fragmentation, caspase-3/7 activity and cytochrome c release into cytosol also confirmed H2O2-me

243 ycle, although rBbKIm triggers apoptosis and cytochrome c release into the cytosol of both cell types

244 y, Bax translocation to the mitochondria and cytochrome C release into the cytosol were increased in

245 so showed p53 translocation to mitochondria, cytochrome c release into the cytosol, and activation of

246 nge in the mitochondrial membrane potential, cytochrome c release into the cytosol, and enhanced casp

247 n induce mitochondrial phospholipid loss and cytochrome c release into WT macrophage cytosol and that

248 his report thus unveils a mechanism by which cytochrome c release is under the opposite control of JN

249 omal cleavage, without affecting the rate of cytochrome c release; JNK inhibition also increased casp

250 ssed, which initiates caspase 8 cleavage and cytochrome c release, leading to apoptosis.

251 pro-apoptotic signals trigger mitochondrial cytochrome c release, leading to caspase activation and

252 In particular, drug-induced Bak activation, cytochrome c release, loss of mitochondrial membrane pot

253 Although cancer cells can be refractory to cytochrome c release, many malignant cells also exhibit

254 ation of nitrated mitochondrial proteins and cytochrome c release, marked apoptosis was detected in t

255 terogeneity, reduced oxygen consumption, and cytochrome c release may underlie apoptosis of retinal e

256 K homo-oligomer formation thereby preventing cytochrome c release-mediated mitochondrial dysfunction.

257 (Q22/S23)) undergo apoptosis as evidenced by cytochrome c release, nuclear fragmentation, and sub-G1

258 p53-induced cytochrome c release occurs through a mechanism involvin

259 stically, Bcl2L12 expression does not affect cytochrome c release or apoptosome-driven caspase-9 acti

260 r through direct inhibition of mitochondrial cytochrome c release or by the action of pan- and pathwa

261 c cells is due to the increase in caspase-3, cytochrome c release, poly(ADP-ribose) polymerase activa

262 ndicated by suppression of etoposide-induced cytochrome c release, poly(ADP-ribose) polymerase cleava

263 eotide phosphate oxidase subunits, cytosolic cytochrome C release, proapoptotic marker lamin expressi

264 terized by cell rounding, membrane blebbing, cytochrome c release, procaspase-3 and poly(ADP-ribose)p

265 tress in mitochondria that eventually led to cytochrome c release, proteolytic activation of caspase

266 fragmentation, mitochondrial depolarization, cytochrome c release, reactive oxygen species generation

267 report that Bid-induced permeabilization and cytochrome c release regularly demonstrate a wave-like p

268 chondria were targeted by mitophagy prior to cytochrome c release, resulting in reduced cellular cyto

269 rthermore, PINK1 expression had no effect on cytochrome c release, suggesting a divergent function fo

270 promote mitochondrial morphology changes and cytochrome c release, suggesting a novel mechanism for h

271 PV antibodies increased cytochrome c release, suggesting damage to mitochondria.

272 apoptosis but did not affect Bid cleavage or cytochrome c release, suggesting that cells die via the

273 ith loss of mitochondrial depolarization and cytochrome c release, suggests a direct attack of the to

274 reased mitochondrial membrane potential, and cytochrome c release that eventually led to cancer cell

275 biochemical characterization, uncovered how cytochrome c releases the autoinhibition of Apaf-1 throu

276 CF-7, estrogen inhibits UV radiation-induced cytochrome C release, the decrease of the mitochondrial

277 transferase dUTP nick-end labeling staining, cytochrome c release, the formation of 4-hydroxy-2-nonne

278 tophagy at the execution stage subsequent to cytochrome c release through caspase 8-mediated cleavage

279 let oxygen, causing mitochondrial damage and cytochrome c release, thus promoting apoptotic cell deat

280 s and that Apaf-1 is only required following cytochrome c release to activate caspases-9/-3.

281 Typically, chemotherapeutics stimulate cytochrome c release to the cytoplasm, thereby activatin

282 process that correlates with LFG blockage of cytochrome c release to the cytosol and caspase activati

283 c overexpression of Pim-1 show inhibition of cytochrome c release triggered by a truncated form of pr

284 tochondrial recruitment of Bax, and increase cytochrome c release upon apoptosis induction.

285 pro-apoptotic proteins and the threshold for cytochrome c release was analyzed.

286 Cytochrome c release was decreased in glucose-free cells

287 y(ADP-ribose) polymerase (PARP) cleavage and cytochrome c release was observed in radiation-exposed E

288 ur in the DMBA/stromal cell-induced pathway, cytochrome c release was stimulated in B cells.

289 To evaluate the role of cytochrome c release, we screened a drug library to iden

290 ly apoptotic events of Bax translocation and cytochrome c release were also delayed.

291 Bax activation and cytochrome c release were independent of caspases; howev

292 cleavage and mitochondrial translocation and cytochrome c release were markedly decreased.

293 Moreover, caspase-8 and Bid activation, and cytochrome c release, were observed, suggesting the exis

294 markers of apoptosis, caspase-3 activity and cytochrome c release, were reduced in the hearts of diab

295 settings, apoptosis occurs by mitochondrial cytochrome c release, which nucleates the Apaf-1/caspase

296 stimuli caused PNPase mobilization following cytochrome c release, which supported an IMS localizatio

297 intrinsic apoptotic pathway characterized by cytochrome c release with caspase-9/-3 activation.

298 ales is primarily triggered by mitochondrial cytochrome c release with subsequent caspase activation.

299 ent with apoptosis, including dose-dependent cytochrome c release, with subsequent caspase-3 and poly

300 elle to matrix swelling, depolarization, and cytochrome c release without inducing cell death.