ライフサイエンスコーパス: apoptosis-inducing factor

1 nic mitochondrial intermembrane protein AIF (apoptosis-inducing factor).

2 lear accumulation of the proapoptotic factor apoptosis inducing factor.

3 apidly swelled and released cytochrome c and apoptosis-inducing factor.

4 ro-apoptotic protein with some similarity to apoptosis-inducing factor.

5 the mitochondrial proteins cytochrome c and apoptosis-inducing factor.

6 me c and Smac/DIABLO, but not the release of apoptosis-inducing factor.

7 This protein was termed S. mansoni-derived apoptosis-inducing factor.

8 chondrial release of cytochrome c (Cyt-c) or apoptosis-inducing factor.

9 otic mitochondrial proteins cytochrome c and apoptosis-inducing factor.

10 ell death similar to the recently identified apoptosis-inducing factor.

11 1-alpha, receptor-interacting protein 1, and apoptosis-inducing factor.

12 endent apoptotic pathway associated with the apoptosis-inducing factor.

13 ents, where it also coincided with increased apoptosis-inducing factor.

14 he release of mitochondrial cytochrome c and apoptosis-inducing factor.

15 xidative stress and mitochondrial release of apoptosis-inducing factor.

16 ion factor, to mature caspase-8, which is an apoptosis-inducing factor.

17 ed intrinsic apoptosis through caspase-3 and apoptosis-inducing factor.

18 dentify an interaction between mitochondrial apoptosis-inducing factor 1 (AIFM1) and adenylate kinase

19 ative phosphorylation and found that dimeric apoptosis-inducing factor 1 (AIFM1) forms a defined comp

20 Apoptosis-inducing factor 1 (AIFM1) is a flavoprotein es

21 cristae density, release of cytochrome C and apoptosis inducing factor, (4) chromatin condensation, n

22 ochondria-derived activator of caspases, and apoptosis-inducing factor, accompanied by a proteolytic

23 The role of apoptosis inducing factor (AIF) in promoting cell death

24 interacted with the mitochondrial localized apoptosis inducing factor (AIF) under both normal and ox

25 Induction in apoptosis inducing factor (AIF) was observed, suggesting

26 Apoptosis Inducing Factor (AIF), a mitochondrial proapop

27 nslocation of mitochondrial cytochrome C and apoptosis inducing factor (AIF), LC3B-positive neurons,

28 Apoptosis-inducing factor (AIF) and AMID (AIF-homologous

29 forms (precursor, mature, and apoptotic) of apoptosis-inducing factor (AIF) and co-localizes with ap

30 Blocking the interaction between the apoptosis-inducing factor (AIF) and cyclophilin A (CypA)

31 hosphorylated Bcl-2, resulting in release of apoptosis-inducing factor (AIF) and cytochrome c from mi

32 the release of proapoptotic factors, such as apoptosis-inducing factor (AIF) and cytochrome c.

33 y, PARP-1-dependent mitochondrial release of apoptosis-inducing factor (AIF) and cytochrome complex (

34 sions of Bax and Bak were enhanced, and both apoptosis-inducing factor (AIF) and endonuclease G (Endo

35 r translocation of the proapoptotic factors, apoptosis-inducing factor (AIF) and endonuclease G (Endo

36 tion, we observed a nuclear translocation of apoptosis-inducing factor (AIF) and endonuclease G in CN

37 cell death involve release of mitochondrial apoptosis-inducing factor (AIF) and its translocation to

38 egulating cellular activities, we identified apoptosis-inducing factor (AIF) as an XIAP binding prote

39 We further show that apoptosis-inducing factor (AIF) cooperated with Bnip3 to

40 , Omi, adenylate kinase-2, cytochrome c, and apoptosis-inducing factor (AIF) during apoptosis and com

41 induced the release of cytochrome c and the apoptosis-inducing factor (AIF) from mitochondria in HL-

42 The translocation of apoptosis-inducing factor (AIF) from mitochondria to the

43 Release of cytochrome c and apoptosis-inducing factor (AIF) from mitochondria was ob

44 but was associated with the translocation of apoptosis-inducing factor (AIF) from the cytoplasm to nu

45 RP) hyperactivation and the translocation of apoptosis-inducing factor (AIF) from the mitochondria to

46 activation is required for translocation of apoptosis-inducing factor (AIF) from the mitochondria to

47 ondria, which was followed by the release of apoptosis-inducing factor (AIF) from the mitochondria, l

48 e Hq mutation as a proviral insertion in the apoptosis-inducing factor (Aif) gene, causing about an 8

49 Genetic mutations in apoptosis-inducing factor (AIF) have a strong associatio

50 r U0126 induced the nuclear translocation of apoptosis-inducing factor (AIF) in A2058 and SKMEL5 cell

51 2 activation in the mitochondrial release of apoptosis-inducing factor (AIF) in cisplatin-treated ren

52 characterized by activation of calpains and apoptosis-inducing factor (Aif) in dying photoreceptors.

53 nd mitochondrial release of cytochrome c and apoptosis-inducing factor (AIF) in the penumbra region w

54 Apoptosis-inducing factor (AIF) is a bifunctional mitoch

55 Mitochondrial apoptosis-inducing factor (AIF) is a central player in t

56 Apoptosis-inducing factor (AIF) is a mitochondrial flavo

57 Apoptosis-inducing factor (AIF) is a mitochondrial flavo

58 Apoptosis-inducing factor (Aif) is a mitochondrial flavo

59 Apoptosis-inducing factor (AIF) is an evolutionarily con

60 We report here that apoptosis-inducing factor (AIF) mediates PARP-1-dependen

61 >T (p.Glu493Val) in AIFM1, the gene encoding apoptosis-inducing factor (AIF) mitochondrion-associated

62 levels, activation, and cleavage, as well as apoptosis-inducing factor (AIF) nuclear translocation an

63 Parthanatos-associated apoptosis-inducing factor (AIF) nuclease (PAAN), also kn

64 The recently discovered mitochondrial apoptosis-inducing factor (AIF) on activation is translo

65 Apoptosis-inducing factor (AIF) promotes cell death yet

66 ource to characterize the mechanism by which apoptosis-inducing factor (AIF) regulates CI biogenesis

67 epsin B function suppressed cell killing and apoptosis-inducing factor (AIF) release from mitochondri

68 caspase-independent cell death, triggered by apoptosis-inducing factor (AIF) release from mitochondri

69 he mechanism of cisplatin-induced apoptosis, apoptosis-inducing factor (AIF) release into the cytosol

70 ptotic factor Bax in mitochondria, while the apoptosis-inducing factor (AIF) remains unchanged.

71 ining intensity and nuclear translocation of apoptosis-inducing factor (AIF) suggesting caspase-indep

72 e newly described roles of MIF is binding to apoptosis-inducing factor (AIF) that "brings" cells to d

73 ility and release of cytochrome c (CytC) and apoptosis-inducing factor (AIF) through upregulation of

74 uggested that the intramitochondrial protein apoptosis-inducing factor (AIF) translocates to the nucl

75 e-3 independent neuronal death that involves apoptosis-inducing factor (AIF) translocation from mitoc

76 e effects through a unique pathway involving apoptosis-inducing factor (AIF) translocation into the n

77 Apoptosis-inducing factor (AIF) was originally discovere

78 Cytosolic cytochrome c and nuclear apoptosis-inducing factor (AIF) were increased 3 h after

79 LH induction increased the activation of apoptosis-inducing factor (AIF), a caspase-independent c

80 Apoptosis-inducing factor (AIF), a mitochondrial oxidore

81 Apoptosis-inducing factor (AIF), a mitochondrial oxidore

82 so were positive for nuclear localization of apoptosis-inducing factor (AIF), an early event in apopt

83 he X-linked AIFM1 gene encodes mitochondrial apoptosis-inducing factor (AIF), an FAD-containing and N

84 -2 phosphorylation, as well as cytochrome c, apoptosis-inducing factor (AIF), and endonuclease G (End

85 spase-3 activation, nuclear translocation of apoptosis-inducing factor (AIF), and induction of p53, a

86 Total and modified caspase-3, Bcl-2, Bad, apoptosis-inducing factor (AIF), and PARP were quantifie

87 ase of the apoptogenic factors cytochrome c, apoptosis-inducing factor (AIF), and proinflammatory hig

88 nd release of cytochrome c, Smac/DIABLO, and apoptosis-inducing factor (AIF), but not endonuclease G.

89 AD(+) depletion and mitochondrial release of apoptosis-inducing factor (AIF), but the causal relation

90 n 80% reduction in the mitochondrial protein apoptosis-inducing factor (AIF), exhibited signs of oxid

91 xecutioner of caspase-independent apoptosis, apoptosis-inducing factor (AIF), from mitochondria is in

92 s was nuclear translocation of mitochondrial apoptosis-inducing factor (AIF), known to trigger both a

93 mitochondrial release of cytochrome c, Smac, apoptosis-inducing factor (AIF), or loss of mitochondria

94 death mediators, including cytochrome c and apoptosis-inducing factor (AIF), was studied in the abse

95 characterized a human gene homologous to the apoptosis-inducing factor (AIF), which is named AIF-like

96 tion of BAX, and release of cytochrome c and apoptosis-inducing factor (AIF), which was translocated

97 AMID is an apoptosis-inducing factor (AIF)-homologous and mitochond

98 mbrane potential, reduced levels of ATP, and apoptosis-inducing factor (AIF)-induced apoptosis.

99 Although hsp70 antagonizes apoptosis-inducing factor (AIF)-mediated cell death, the

100 L2 accumulates in the nucleus, together with apoptosis-inducing factor (AIF).

101 , and had defective nuclear translocation of apoptosis-inducing factor (AIF).

102 s was determined by nuclear translocation of apoptosis-inducing factor (AIF).

103 ors, including cytochrome c, Smac/DIABLO and apoptosis-inducing factor (AIF).

104 HtrA2/Omi but not endonuclease G (EndoG) and apoptosis-inducing factor (AIF).

105 s of the mitochondrial import oxidoreductase apoptosis-inducing factor (AIF).

106 ts enigmatic interaction with oxidoreductase Apoptosis-inducing factor (AIF).

107 APN1-induced cleavage of mitochondrial-bound apoptosis-inducing factor (AIF).

108 resulting in the release of cytochrome c and apoptosis-inducing factor (AIF).

109 lity transition and nuclear translocation of apoptosis-inducing factor (AIF).

110 by poly(ADP-ribose) polymerase (PARP-1) and apoptosis-inducing factor (AIF).

111 dependent type of neuronal PCD involving the apoptosis-inducing factor (AIF).

112 r a caspase-independent mechanism, involving apoptosis-inducing factor (AIF).

113 Liberibacter solanacearum": the apoptosis-inducing factor AIF3 was downregulated in LsoA

114 with the identified mitochondrion-associated apoptosis inducing factor (AIFM1) have roles in the indu

115 imary rod loss was linked to upregulation of apoptosis-inducing factor, although only a minute fracti

116 ells by a pathway involving translocation of apoptosis-inducing factor and caspase 12 to the nucleus.

117 d with the expression of apoptotic proteins (apoptosis-inducing factor and cleaved caspase-3) and aut

118 mitochondrial depolarization and release of apoptosis-inducing factor and cytochrome c Furthermore,

119 s induced in both cell types, but release of apoptosis-inducing factor and endonuclease G was detecte

120 ential, parylation, nuclear translocation of apoptosis-inducing factor and endonuclease G, and supra-

121 les released from the mitochondrion, such as apoptosis-inducing factor and endonuclease G, may induce

122 CIMD also depends on apoptosis-inducing factor and endonuclease G, which are

123 tion) prevented intranuclear localization of apoptosis-inducing factor and protected neurons from exc

124 nd by assessing the mitochondrial release of apoptosis-inducing factor and Smac/DIABLO.

125 itment of mitochondrial caspase-independent (apoptosis-inducing factor) and caspase-dependent (Smac/D

126 oteins (e.g., cytochrome c, Smac/DIABLO, and apoptosis-inducing factor), and caspase activation.

127 o induce directly the release of Cyt c, AIF (apoptosis-inducing factor), and Smac (second mitochondri

128 ytoplasmic translocation of cytochrome c and apoptosis inducing factor, and active caspases 3 and 7,

129 lease of mitochondrial proapoptotic factors, apoptosis inducing factor, and endonuclease G.

130 on, oxidant stress, mitochondrial release of apoptosis inducing factor, and nuclear DNA fragmentation

131 to mitochondria, release of cytochrome c and apoptosis-inducing factor, and activation of caspase-9 a

132 ed by the release of mitochondrial proteins, apoptosis-inducing factor, and cytochrome c.

133 ation, cytosolic release of cytochrome c and apoptosis-inducing factor, and mitochondrial membrane po

134 d cellular respiration, prevented release of apoptosis-inducing factor, and reduced neuronal cell dea

135 reduced the leakage of both cytochrome c and apoptosis-inducing factor, and significantly improved ce

136 To identify partially the apoptosis inducing factor, aqueous humor was pretreated

137 abolished CCK-induced caspase 3 activation, apoptosis-inducing factor, as well as X-linked inhibitor

138 se-3 activation and mitochondrial release of apoptosis-inducing factor at low microM concentrations.

139 Total and modified apoptosis-inducing factor, Bcl-2 family proteins, phosph

140 r of apoptotic cells and expression of total apoptosis-inducing factor, Bcl-2, Bak, and Bax in the pr

141 optosis and key apoptotic mediators, such as apoptosis-inducing factor, caspase 3, caspase 8, caspase

142 levels of Bcl-2 and increased expression of apoptosis-inducing factor, caspase-3, and cleavage of BI

143 of bacterial meningitis and induces a novel apoptosis-inducing factor-dependent (AIF-dependent) form

144 ed cell death proceeded predominately via an apoptosis-inducing factor-dependent pathway in XY neuron

145 but not other mitochondrial related factors (apoptosis-inducing factor, endonuclease G, and HtrA2/Omi

146 ted with mitochondria, and cytochrome c, and apoptosis-inducing factor escaped from mitochondria to t

147 city in parental cells, whereas knockdown of apoptosis-inducing factor expression suppressed lapatini

148 a pan-caspase inhibitor and by knockdown of apoptosis-inducing factor expression.

149 by releasing cytochrome c and translocating apoptosis inducing factor from mitochondria to the nucle

150 he release of cytochrome c, Smac/DIABLO, and apoptosis inducing factor from mitochondria, and reduced

151 and Bax and the release of cytochrome c and apoptosis inducing factor from mitochondria.

152 ndrial membrane permeability, and release of apoptosis-inducing factor from mitochondria are partiall

153 in A and NAD(+) blocked translocation of the apoptosis-inducing factor from mitochondria to nuclei, a

154 ne triphosphate levels, and translocation of apoptosis-inducing factor from mitochondria to the nucle

155 poly(ADP-ribose) (PAR)-dependent release of apoptosis-inducing factor from mitochondria, leading to

156 arly step before release of cytochrome c and apoptosis-inducing factor from mitochondria.

157 n of mitochondrial mu-calpain and release of apoptosis-inducing factor from the mitochondrial interme

158 y is necessary for the complete discharge of apoptosis-inducing factor from the mitochondrial interme

159 ic suppression of caspase 4, cathepsin B, or apoptosis-inducing factor function significantly suppres

160 a positive feedback loop with Dronc and the apoptosis-inducing factors Hid and Reaper.

161 AMID (apoptosis-inducing factor-homologous mitochondrion-assoc

162 demonstrates recruitment of Smac/Diablo and apoptosis-inducing factor in chronic neurodegeneration.

163 caspase-3-dependent nuclear translocation of apoptosis-inducing factor in NMDA-treated neurons and re

164 s by a mechanism independent of caspase- and apoptosis-inducing factor in nonproliferating U937 cells

165 ient cells failed to release cytochrome c or apoptosis-inducing factor in response to recombinant Bax

166 istant cells did not release cytochrome c or apoptosis-inducing factor in response to recombinant Bax

167 ve mitochondrial oxidative damage, releasing apoptosis-inducing factor into cytosol.

168 immunolabeling and in cytosolic and nuclear apoptosis-inducing factor labeling within 60 min.

169 electrophoresis, suggesting a predominantly apoptosis-inducing factor-mediated cell death process.

170 is no information on whether Smac/Diablo or apoptosis-inducing factor might play a role in chronic n

171 thermore, we found that NS7a interacted with apoptosis-inducing factor mitochondria associated 1 (AIF

172 ADS-CoV suppresses IFN-lambda production via apoptosis-inducing factor mitochondria associated 1 (AIF

173 We found that the flavoprotein apoptosis-inducing factor mitochondria-associated 2 (AIF

174 ressor protein 1 (FSP1) (previously known as apoptosis-inducing factor mitochondrial 2 (AIFM2)) as a

175 he mitochondrial release of cytochrome c and apoptosis-inducing factor, mitochondrial membrane depola

176 , Bax/Bcl-xL-dependent apoptosis pathway and apoptosis inducing factor nuclear translocation were all

177 y(ADP-ribose) polymerase) cleavage, and AIF (apoptosis-inducing factor) nuclear translocation.

178 ch as the induction of autophagy, release of apoptosis-inducing factor, or opening of the mitochondri

179 interfering RNA to reduce the expression of apoptosis-inducing factor partially inhibited CDDO-induc

180 appears to occur by a caspase 3-independent apoptosis-inducing factor pathway.

181 omponent of biphenyl dioxygenase (BphA4) and apoptosis-inducing factor, Pdr lacks one of the arginine

182 After CP/Rep, the amount of apoptotic cells, apoptosis-inducing factor, phospho-Bad, phospho-PKC-alph

183 ermeability transition, and cytochrome C and apoptosis-inducing factor release from isolated mitochon

184 ential, Bax translocation, cytochrome c, and apoptosis-inducing factor release) and apoptosis by imat

185 caspase activation) and caspase-independent (apoptosis-inducing factor release) pathways, and limited

186 /direct IAP binding protein with low pI, and apoptosis-inducing factor release), caspase activation,

187 damage (e.g., cytochrome c, Smac/DIABLO, and apoptosis-inducing factor release), caspase activation,

188 mitochondrial dysfunction (cytochrome c and apoptosis-inducing factor release), caspase-3 and -8 act

189 mitochondrial dysfunction (cytochrome c and apoptosis-inducing factor release), caspase-3 and -8 act

190 y but significantly reduced cytochrome c and apoptosis-inducing factor release, loss of mitochondrial

191 is initiated by the mitochondrial release of apoptosis-inducing factor, resulting in caspase-independ

192 and causing the release of cytochrome c and apoptosis-inducing factor, resulting in DNA fragmentatio

193 gesting that expression and/or export of the apoptosis-inducing factor(s) is regulated by the dot/icm

194 The presence of cleaved apoptosis inducing factor (tAIF) and the absence of acti

195 resulted in less cytochrome c and truncated apoptosis inducing factor (tAIF) release from mitochondr

196 ondrial release and nuclear translocation of apoptosis-inducing factor to initiate chromatinolysis an

197 l, caspases activation, the translocation of apoptosis-inducing factor to the nucleus, and DNA fragme

198 oly(ADP-ribose) polymerase, translocation of apoptosis-inducing factor to the nucleus, and morphologi

199 al membrane permeability or translocation of apoptosis-inducing factor to the nucleus.

200 Csf2, Il6, and Egf and up-regulation of the apoptosis-inducing factor Trail in the oviduct.

201 Although mitochondrial dysfunction and apoptosis-inducing factor translocation from the mitocho

202 or PARP-1-induced mitochondrial dysfunction, apoptosis-inducing factor translocation, and subsequent

203 However, apoptosis-inducing factor was released from mitochondria

204 in Bax, and release from mitochondria of the apoptosis-inducing factor were selectively abrogated in

205 ondrial depolarization and relocalization of apoptosis-inducing factor, whereas the BRAF-V600E-mutate

206 creased release and nuclear translocation of apoptosis-inducing factor with subsequent cell death.

207 t of activation of caspases-1, -3, and -8 or apoptosis-inducing factor within MNs, with a blockade of