ライフサイエンスコーパス: AIF

1 AIF had lower selectivities than traditional LC-MS/MS, p

2 AIF has been known to have both apoptotic and metabolic

3 AIF is an FAD-dependent NADH oxidase that is imported in

4 AIF stability is markedly reduced in Scythe(-/-) cells,

5 AIF translocates to the host cell nucleus, implying that

6 AIF was found to be a target of XIAP-mediated ubiquitina

7 AIF was required for recruitment of MIF to the nucleus,

8 AIF-1 in the skin and lung tissues of patients with SSc

9 AIF-1 isoform expression in response to TGFbeta and inte

10 AIF-1 protein was present in affected vessels of the lun

11 AIF-1 significantly increased Jurkat T cell migration to

12 Allograft inflammatory factor 1 (AIF-1) was first identified in rat cardiac allografts un

13 Allograft inflammatory factor 1 (AIF-1), a protein initially identified in chronically re

14 ably transfected Jurkat T cells expressing 2 AIF-1 splicing variants were prepared, and their migrati

15 Although AIF release also was caspase-independent and commenced w

16 Although AIF was originally discovered as a caspase-independent c

17 Apoptosis-inducing factor (AIF) and AMID (AIF-homologous mitochondrion-associated inducer of death

18 These results reveal PAR polymer as an AIF-releasing factor that plays important roles in PARP-

19 nsible for apoptosis in MCL cells because an AIF inhibitor, but not pan-caspase or paspase-9 inhibito

20 Here we identified an AIF-interacting protein, CHCHD4, which is the central co

21 Percentage method), activation of PARP-1 and AIF.

22 nd ischemic stress, levels of both AKIP1 and AIF were enhanced.

23 BID and with suppression of cathepsin B and AIF release into the cytosol.

24 the core cells mediated by HIFs, Bnip3, and AIF.

25 ng pathways (eg, release of cytochrome c and AIF from mitochondria, cleavage of caspase-9 and -8).

26 affects susceptibility of AIF to calpain and AIF-DNA interaction, the two events critical for initiat

27 expression of the microglial genes CD11b and AIF-1 and was modestly increased with AD status and the

28 PARP-1 cleavage and AIF expression were also increased in astrocytes in NBD

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

30 ased levels of cytochrome c, Smac/DIABLO and AIF in the cytosol while their levels were decreased in

31 of cytochrome c, Smac/DIABLO, Omi/HtrA2, and AIF but not endonuclease G.

32 deviation (Vx0%) of 7.2% compared to MS and AIF-MS with LOQs of 1.24-4.32 ng muL(-1) and relative pr

33 s a combination of ferroptosis, necrosis and AIF-dependent apoptosis.

34 gnificantly reduced VDAC oligomerization and AIF release.

35 unohistochemistry was performed for PARP and AIF.

36 hosphorylation, hyperactivation of PARP, and AIF translocation to the nucleus.

37 The apoptotic responses and AIF release were caspase-independent, as they were not b

38 njury and release of cytochrome c, Smac, and AIF into the cytosol and caspase-9, caspase-3, caspase-7

39 chondrial release of cytochrome c, Smac, and AIF.

40 plasia and suggest that oxidative stress and AIF may be promising therapeutic targets.

41 ondrial membrane permeability transition and AIF release.

42 of the subcellular localization of TULA and AIF together with the functional analysis of TULA mutant

43 tive oxygen species (ROS), and when XIAP and AIF were expressed in combination, a cumulative decrease

44 nput function [AIF] for CT, population-based AIF for MR imaging; temporal sampling rate of 0.5 second

45 lls primarily via a caspase-independent, Bax/AIF/Endo G pathway.

46 Blocking AIF translocation resulted in a decreased apoptosis, sug

47 ments revealed that XIAP interacts with both AIF forms.

48 cisplatin, and 4-TBP were not compromised by AIF knockdown, even in the presence of zVAD-fmk.

49 , and monitoring of product ions obtained by AIF-MS.

50 ent-rich conditions is largely unaffected by AIF ablation.

51 Four of the selected 10 candidates (AIF, cyclic AMP-responsive element binding protein, ephr

52 w that both forms of oxidative stress caused AIF to be cleaved with the product located to the cytoso

53 In mammalian cells, AIF is released from mitochondria in response to apoptot

54 However, under growth stress conditions, AIF depletion from DU145 and PC3 cell lines led to signi

55 Consequently, AIF deficiency expanded neovascularization and diminishe

56 l modeling was performed using the corrected AIF.

57 The helical CT AIF can be used to improve the semiquantitative assessme

58 We previously demonstrated AIF-1 expression in inflammatory cells infiltrating skin

59 rades PAR polymer, prevents PARP-1-dependent AIF release.

60 nhibitory factor (MIF) as a PARP-1-dependent AIF-associated nuclease (PAAN).

61 er, these results define calpain I-dependent AIF release as a novel signaling pathway that mediates n

62 AR, is essential in regulating PAR-dependent AIF release from mitochondria and parthanatos.

63 is inhibition, mitochondrial depolarization, AIF translocation, and neuron death, independent of PARP

64 -registered multidetector helical CT-derived AIF (3086 + or - 941) (P = .90).

65 e (AUC) for dynamic multidetector CT-derived AIF (3108 + or - 1250 [standard deviation]) and that for

66 ondrial apoptotic factors (i.e. Smac/DIABLO, AIF, and endoglycosidase G).

67 ion may be functionally important and enable AIF to act as a redox-signaling molecule linking NAD(P)H

68 function in AIF-deficient cells and enabled AIF-deficient embryoid bodies to undergo cavitation, a p

69 hypomorphic mutations of the genes encoding AIF or Apaf-1.

70 dial AD normalized to the AUC for the entire AIF was significant (R(2) = 0.82, P <.001).

71 othelial cells in affected tissues expressed AIF-1.

72 Apoptosis-inducing factor (AIF) and AMID (AIF-homologous mitochondrion-associated i

73 ing in release of apoptosis-inducing factor (AIF) and cytochrome c from mitochondria and activation a

74 factors, such as apoptosis-inducing factor (AIF) and cytochrome c.

75 ndrial release of apoptosis-inducing factor (AIF) and cytochrome complex (Cyt c) is reduced in Glu(-)

76 nhanced, and both apoptosis-inducing factor (AIF) and endonuclease G (Endo G) were released from the

77 poptotic factors, apoptosis-inducing factor (AIF) and endonuclease G (EndoG), through p53-dependent u

78 translocation of apoptosis-inducing factor (AIF) and endonuclease G in CNGA3(-/-)/Nrl(-/-) and CNGB3

79 of mitochondrial apoptosis-inducing factor (AIF) and its translocation to the nucleus, which results

80 es, we identified apoptosis-inducing factor (AIF) as an XIAP binding protein.

81 further show that apoptosis-inducing factor (AIF) cooperated with Bnip3 to promote lumen clearance.

82 cytochrome c, and apoptosis-inducing factor (AIF) during apoptosis and compared the release with that

83 translocation of apoptotis-inducing factor (AIF) followed by irreversible caspase-independent cell d

84 translocation of apoptosis-inducing factor (AIF) from the mitochondria to the nucleus.

85 translocation of apoptosis-inducing factor (AIF) in A2058 and SKMEL5 cells, and the introduction of

86 The role of apoptosis inducing factor (AIF) in promoting cell death versus survival remains con

87 cytochrome c and apoptosis-inducing factor (AIF) in the penumbra region were reduced by NBP.

88 Apoptosis-inducing factor (AIF) is a bifunctional mitochondrial flavoprotein critic

89 Mitochondrial apoptosis-inducing factor (AIF) is a central player in the caspase-independent cell

90 Apoptosis-inducing factor (AIF) is a mitochondrial flavoprotein that, beyond its ap

91 Apoptosis-inducing factor (AIF) is a mitochondrial flavoprotein with dual roles in

92 Apoptosis-inducing factor (AIF) is an evolutionarily conserved, ubiquitously expres

93 the gene encoding apoptosis-inducing factor (AIF) mitochondrion-associated 1.

94 avage, as well as apoptosis-inducing factor (AIF) nuclear translocation and executioner caspase 3 act

95 Apoptosis-inducing factor (AIF) promotes cell death yet also controls mitochondrial

96 ath, triggered by apoptosis-inducing factor (AIF) release from mitochondria and its translocation to

97 cell killing and apoptosis-inducing factor (AIF) release from mitochondria.

98 nduced apoptosis, apoptosis-inducing factor (AIF) release into the cytosol was observed, and the unde

99 ondria, while the apoptosis-inducing factor (AIF) remains unchanged.

100 translocation of apoptosis-inducing factor (AIF) suggesting caspase-independent cell death.

101 chondrial protein apoptosis-inducing factor (AIF) translocates to the nucleus and promotes caspase-in

102 ath that involves apoptosis-inducing factor (AIF) translocation from mitochondria to the nucleus and

103 pathway involving apoptosis-inducing factor (AIF) translocation into the nucleus.

104 ondrial localized apoptosis inducing factor (AIF) under both normal and oxidant stress.

105 Induction in apoptosis inducing factor (AIF) was observed, suggesting a parallel caspase-indepen

106 ome c and nuclear apoptosis-inducing factor (AIF) were increased 3 h after OGD, and the translocation

107 the activation of apoptosis-inducing factor (AIF), a caspase-independent cell death constituent activ

108 Apoptosis-inducing factor (AIF), a mitochondrial oxidoreductase, is released into t

109 des mitochondrial apoptosis-inducing factor (AIF), an FAD-containing and NADH-specific oxidoreductase

110 as cytochrome c, apoptosis-inducing factor (AIF), and endonuclease G (EndoG) release.

111 se-3, Bcl-2, Bad, apoptosis-inducing factor (AIF), and PARP were quantified by immunoblotting.

112 ors cytochrome c, apoptosis-inducing factor (AIF), and proinflammatory high-mobility group protein B1

113 Smac/DIABLO, and apoptosis-inducing factor (AIF), but not endonuclease G.

114 ndrial release of apoptosis-inducing factor (AIF), but the causal relationships between these two eve

115 chondrial protein apoptosis-inducing factor (AIF), exhibited signs of oxidative stress and progressiv

116 cytochrome c and apoptosis-inducing factor (AIF), which was translocated to the nucleus.

117 AMID is an apoptosis-inducing factor (AIF)-homologous and mitochondria-associated protein that

118 evels of ATP, and apoptosis-inducing factor (AIF)-induced apoptosis.

119 hsp70 antagonizes apoptosis-inducing factor (AIF)-mediated cell death, the relative importance of pre

120 rase (PARP-1) and apoptosis-inducing factor (AIF).

121 PCD involving the apoptosis-inducing factor (AIF).

122 hanism, involving apoptosis-inducing factor (AIF).

123 translocation of apoptosis-inducing factor (AIF).

124 translocation of apoptosis-inducing factor (AIF).

125 us, together with apoptosis-inducing factor (AIF).

126 cytochrome c and apoptosis-inducing factor (AIF).

127 translocation of apoptosis-inducing factor (AIF).

128 t discovered four ATBS1-Interacting Factors (AIFs) that are members of another atypical bHLH protein

129 lycolytic inhibition, mitochondrial failure, AIF translocation, and neuron death that otherwise resul

130 e analysis performed on selected samples for AIF correction.

131 ction of a small interfering RNA (siRNA) for AIF partially protected these cells from BAY 43-9006-ind

132 ned 2.9-fold higher acid-insoluble fraction (AIF) and 2.3-fold more condensed tannins; both are relat

133 py, full-scan MS, and all-ion fragmentation (AIF) MS were compared.

134 ), as well as MS upon all-ion fragmentation (AIF-MS).

135 r in combination with all-ion-fragmentation (AIF), data-independent-acquisition (DIA), and data-depen

136 ns for precursor ions and all ion fragments (AIF) were employed with a generic gradient LC method to

137 so observed that peritoneal macrophages from AIF-deficient mice showed anti-apoptotic survival compar

138 Conditioned media from AIF-1-expressing clones stimulated synthesis of types I

139 ected to derive the arterial input function (AIF), with high-performance liquid chromatography radiom

140 e derived (measured arterial input function [AIF] for CT, population-based AIF for MR imaging; tempor

141 These findings explain how AIF contributes to the biogenesis of respiratory chain c

142 However, AIF, but not activation of caspases or PARP, was respons

143 In healthy cells, mature human AIF lacks only the first 54 amino acids, differing signi

144 e investigated the redox properties of human AIF and AMID by comparing them with yeast Ndi1, a type 2

145 aracterize four pathologic variants of human AIF: V243L, G262S, G308E, and G338E.

146 These results identify AIF as a new XIAP binding partner and indicate a role fo

147 Averting apoptosis in AIF-deficient mice decreased apoptosis of leukocytes and

148 th diabetic nephropathy showed a decrease in AIF within the renal tubular compartment and lower AIFM1

149 eostasis, we hypothesized that a decrease in AIF would result in chronic kidney disease (CKD).

150 Deficiency in AIF is known to result in defective oxidative phosphoryl

151 Mice deficient in AIF also exhibit quantitatively normal PCD of postmitoti

152 rotein reestablished respiratory function in AIF-deficient cells and enabled AIF-deficient embryoid b

153 d VEGF-induced corneal neovascularization in AIF-deficient mice.

154 ratory defect that mimicked that observed in AIF-deficient cells.

155 temic sclerosis (SSc) with a polymorphism in AIF-1 isoform 2.

156 CHCHD4 levels could be restored in AIF-deficient cells by enforcing its AIF-independent mit

157 Bnip3 silencing in AIF-null EBs nearly blocked apoptosis and cavitation.

158 effect in A375 cells, in which drug-induced AIF release was negligible.

159 ession in neurons prevented ischemia-induced AIF translocation.

160 hibiting gamma-H2AX, which in turn inhibited AIF changes in Ad.5/3-CTV-infected neuroblastoma cells.

161 Inhibiting AIF rescued neuroblastoma cells from Ad.5/3-CTV-induced

162 er ischemia and to cleave intramitochondrial AIF near its N terminus.

163 The purpose of this study was to investigate AIF-1 expression in affected tissues from patients with

164 mpanied by a conformational change involving AIF-specific N-terminal and regulatory 509-559 peptides

165 Isolated AIF and AMID containing naturally incorporated FAD displ

166 However, after reconstituting isolated AIF or AMID into bacterial or mitochondrial membranes, N

167 ored in AIF-deficient cells by enforcing its AIF-independent mitochondrial localization.

168 fibroblasts, thymocytes and B cells lacking AIF underwent normal death.

169 from mitochondria versus sequestering leaked AIF in the cytosol remains controversial.

170 p70 mutant co-immunoprecipitated with leaked AIF in injured cells and decreased nuclear AIF accumulat

171 However, despite a 50% lower AIF protein content in the kidney cortex, there was no l

172 Also, there was an increase in mature AIF (57 kDa) levels (1.22+/-0.01-fold; P<0.05) and a tre

173 tandard deviations of interday measurements, AIF was concluded to be the method of choice for concent

174 stituent activated by Bid, and mitochondrial AIF expression was attenuated by chronic BI-11A7 infusio

175 a-driven Bnip3 generation, and mitochondrial AIF release.

176 an insult sufficient to cause mitochondrial AIF release, nuclear AIF accumulation, and apoptosis.

177 PAR polymer induces mitochondrial AIF release and translocation to the nucleus.

178 glycolytic failure upstream of mitochondrial AIF release.

179 deltaATPase) failed to prevent mitochondrial AIF release.

180 ted bax activation and reduced mitochondrial AIF release after injury.

181 Moreover AIF-deficient PC3 cells exhibited substantial reduction

182 Moreover, AIF also regulated Bnip3 expression through mitochondria

183 Our study showed that naturally folded mouse AIF very slowly reacts with NAD(P)H (k cat of 0.2-0.01 s

184 forms of naturally folded recombinant murine AIF.

185 because neuronal transfection of the mutant AIF resistant to calpain cleavage was not released after

186 Upon reduction with NADH, AIF undergoes dimerization and forms tight, long-lived F

187 d AIF in injured cells and decreased nuclear AIF accumulation.

188 m and furthermore, failed to prevent nuclear AIF accumulation.

189 to cause mitochondrial AIF release, nuclear AIF accumulation, and apoptosis.

190 neural tube closure occur in the absence of AIF, indicating that Aif function is not required for ap

191 dentified calpain I as a direct activator of AIF release in neuronal cultures challenged with oxygen-

192 tions in the structure and redox activity of AIF G262S, on the other hand, were more severe than coul

193 and redox balance, the enzymatic activity of AIF is critical for this support.

194 demonstrated that the enzymatic activity of AIF is required for aggressive growth.

195 he expression level or/and redox activity of AIF tends to cause an early and severe neurodegeneration

196 Partial blocking of AIF release by cyclosporine A in OmpU-treated cells furt

197 s study we have explored the contribution of AIF to the progression of prostate cancer.

198 a that TULA enhances the apoptotic effect of AIF by facilitating the interactions of AIF with its apo

199 was undertaken to investigate the effects of AIF-1 on T cell migration and production of cytokines ca

200 Expression of AIF-1 isoform 2 in Jurkat T cells up-regulated their pro

201 nd significant increase in the expression of AIF-1 isoform 2 transcripts (P < 0.005), which was due t

202 translocation and intensified expression of AIF.

203 The timing and extent of AIF release makes it unlikely that it is involved in the

204 contributed over two-thirds of the fluxes of AIF and condensed tannins to soil.

205 nexpected link between the vital function of AIF and the propensity of cells to undergo apoptosis.

206 s were detected in the structure/function of AIF V243L and G338E, respectively, indicating that a mar

207 hat both normal and apoptogenic functions of AIF are controlled by NADH.

208 ctivities are coordinated, and the impact of AIF upon human disease, in particular cancer, is not wel

209 t of AIF by facilitating the interactions of AIF with its apoptotic co-factors, which remain to be id

210 of very few known functional interactors of AIF.

211 Three well-characterized isoforms of AIF-1 result from alternative messenger RNA (mRNA) splic

212 Knockdown of AIF by shRNA rescues the radiosensitization induced by E

213 verexpression of calpastatin or knockdown of AIF expression conferred neuroprotection against cell de

214 While RNA interference-mediated knockdown of AIF protected melanocytes against apoptosis induced by s

215 Cells with reduced levels of AIF are resistant to PARP-1-dependent cell death and PAR

216 We report that the loss of AIF in fibroblasts led to mitochondrial electron transpo

217 lastoma cells mediated through modulation of AIF, ATM, and gamma-H2AX.

218 Depletion or hypomorphic mutation of AIF caused a downregulation of CHCHD4 protein by diminis

219 eintroduction of Scythe or overexpression of AIF in Scythe(-/-) cells restores their sensitivity to a

220 ically damaging both the redox properties of AIF and mitochondrial respiration.

221 ver, there was significant redistribution of AIF from mitochondria to the nucleus.

222 hese data implicate Scythe as a regulator of AIF.

223 poptosis as well as mitochondrial release of AIF and cytochrome c, and subsequent activation of caspa

224 the cytoplasm, thereby preventing release of AIF from mitochondria and its accumulation in the nucleu

225 al dysfunction, and BID-dependent release of AIF from mitochondria, and whose lethality is enhanced b

226 rom the lysosomal compartment and release of AIF from mitochondria.

227 tion and release of mitochondrial release of AIF, cytochrome c, and Smac induced by UVB.

228 a cell death signal that induces release of AIF.

229 Finally, restoration of AIF-deficient PC3 cells with AIF variants demonstrated t

230 However, the role of AIF in mitochondrial respiration and redox metabolism ha

231 ese studies suggest that the primary role of AIF relates to complex I function, with differential eff

232 t cell death effector, bioenergetic roles of AIF, particularly relating to complex I functions, have

233 Our findings expand the spectrum of AIF-related disease and provide insight into the effects

234 < 0.005), which was due to stabilization of AIF-1 isoform 2 mRNA.

235 d tissues and to the specific stimulation of AIF-1 isoform 2 by TGFbeta.

236 Suppression of AIF expression in the prostate cancer cell lines LNCaP,

237 te His 453, and it affects susceptibility of AIF to calpain and AIF-DNA interaction, the two events c

238 ased 3 h after OGD, and the translocation of AIF from mitochondria to nucleus was partly blocked by t

239 tosis, while preventing the translocation of AIF from mitochondria to the nucleus as well as the acti

240 atio, inhibition of nuclear translocation of AIF, and attenuated cytochrome c release in cytosol.

241 ediated through the nuclear translocation of AIF.

242 The truncation of AIF by calpain activity appeared to be essential for its

243 the dependency of T cells versus B cells on AIF for function and survival correlated with their meta

244 show that T cells, but not B cells, rely on AIF to maintain mitochondrial electron transport and tha

245 h phosphate analogs BeF(3)(-), VO(4)(3-), or AIF(4)(-), were determined to 2.2- to 2.4-A resolution.

246 Expression of either XIAP or AIF attenuated both basal and antimycin A-stimulated lev

247 pendent mitochondrial membrane permeability, AIF translocation, and neuron death.

248 Two of these predictions, AIF-1 and SMN1, were selected for further experimental a

249 te are transmitted to the surface, promoting AIF dimerization and restricting access to a primary nuc

250 TULA binds to the apoptosis-inducing protein AIF, which has previously been shown to function as a ke

251 ptogenic mitochondrial intermembrane protein AIF (apoptosis-inducing factor).

252 lowing deletion of the mitochondrial protein AIF, OPA1, or PINK1, as well as chemical inhibition of t

253 well as mitochondrial intermembrane proteins AIF and Mia40.

254 educed expression of pro-apoptotic proteins (AIF and Bax).

255 athway involving autophagy and not requiring AIF.

256 e ATPase domain is critical for sequestering AIF in the cytosol.

257 mitochondrial membranes, N-terminally tagged AIF and AMID displayed substantial NADH:O(2) activities

258 Overexpressing N-terminally tagged AIF and AMID enhanced the growth of a double knock-out E

259 -binding site mutants of N-terminally tagged AIF and AMID failed to show both NADH:O(2) activity and

260 the redox activities of N-terminally tagged AIF and AMID were sensitive to rotenone, a well known co

261 In contrast, C-terminally tagged AIF and NADH-binding site mutants of N-terminally tagged

262 enhances activation of lymphocytes, and that AIF-1 expression in activated lymphocytes may have impor

263 These studies demonstrate that AIF deficiency is a risk factor for the development of d

264 Using RNA interference, we demonstrate that AIF is essential for the apoptotic effect of TULA.

265 ines LNCaP, DU145, and PC3 demonstrated that AIF does not contribute to cell toxicity via a variety o

266 hival gene expression data demonstrated that AIF transcript levels are elevated in human prostate can

267 in human prostate cancer, and we found that AIF protein is increased in prostate tumors.

268 These data indicate that AIF-1 is expressed in activated T lymphocytes, that its

269 We propose that AIF and AMID are previously unidentified mammalian NDH-2

270 Overall these studies show that AIF is an important factor for advanced prostate cancer

271 These results suggest that AIF-1 may participate in the early pathogenesis of SSc b

272 These data suggest that AIF-1 plays an important role in the pathogenesis of SSc

273 Our data suggest that AIF-related apoptosis plays an important role in neovasc

274 ed in a decreased apoptosis, suggesting that AIF contributes to gossypol-mediated cytotoxicity in CLL

275 The AIF method achieved a lower limit of detection of 0.85 n

276 The AIF siRNA had little effect in A375 cells, in which drug

277 The AIF was reconstructed by using a combination of bolus-tr

278 After the AIF reconstruction method was validated in healthy anima

279 Myocardial AD normalized to the AUC for the AIF measured during helical multidetector CT correlated

280 sets of fragment ions were evaluated for the AIF method.

281 tion, whereas less pronounced changes in the AIF properties could lead to a broad range of slowly pro

282 elical imaging enables reconstruction of the AIF during multidetector CT perfusion imaging.

283 sis was induced mainly via activation of the AIF pathway.

284 rted here alters the redox properties of the AIF protein and results in increased cell death via apop

285 AD) parameters normalized to portions of the AIF were compared with microsphere myocardial blood flow

286 Depletion of MIF, disruption of the AIF-MIF interaction, or mutation of glutamic acid at pos

287 lation between the mutational effects on the AIF function and clinical phenotype was observed only fo

288 dosomes containing uPAS cargo and leading to AIF-mediated necrotic cell death.

289 How PARP-1 activation leads to AIF release is not known.

290 and late endosomes by 4- to 5-fold prior to AIF nuclear translocation and subsequent glioma demise.

291 erence to the microglial-specific transcript AIF-1 revealed an increase in this transcript in MS.

292 ax/Bak/Bcl-2 signaling cascade that triggers AIF/EndoG-mediated apoptosis in colon cancer cells.

293 When AIF analysis was applied to helical multidetector CT myo

294 However, the mechanism by which AIF is released from mitochondria after neuronal injury

295 the AIFM1-related disorders depend on which AIF feature is predominantly affected (i.e., cellular pr

296 restoration of AIF-deficient PC3 cells with AIF variants demonstrated that the enzymatic activity of

297 ast, hsp70-deltaATPase did not interact with AIF either in intact cells or in a cell-free system and

298 ant displayed a more robust interaction with AIF.

299 Scythe physically interacts with AIF and regulates its stability.

300 repeat 2 of XIAP is sufficient for the XIAP/AIF interaction, which is disrupted by Smac/DIABLO.