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 1-alpha, receptor-interacting protein 1, 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 endent apoptotic pathway associated with the apoptosis-inducing factor.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

43 2 activation in the mitochondrial release of apoptosis-inducing factor (AIF) in cisplatin-treated ren

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

65 Apoptosis-inducing factor (AIF) was originally discovere

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

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

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

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

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

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

72 -2 phosphorylation, as well as cytochrome c, apoptosis-inducing factor (AIF), and endonuclease G (End

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

177 However, apoptosis-inducing factor was released from mitochondria

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

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

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

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