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 knockdown reduced STS-induced apoptosis in both of 1

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

6 AIF translocates to the host cell nucleus, implying that

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

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

9 AIF was significantly higher in the AgP (P = 0.07) and C

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

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

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

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

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

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

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

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

21 ed intrinsic pathway involving caspase-9 and AIF, and the extrinsic pathway involving caspase-8 are s

22 ase, this study evaluated caspase-8, -9, and AIF in periodontal disease.

23 Levels of caspase-8, -9, and AIF were evaluated in gingival crevicular fluid (GCF) of

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

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

26 nslocation of mitochondrial cytochrome C and AIF was significantly alleviated in the 0.7 g/kg/d ethan

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

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

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

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

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

32 A(m) and AIF were determined radiometrically for comparison.

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

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

35 gnificantly reduced VDAC oligomerization and AIF release.

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 that 16E6, but not 6E6, suppressed apoptotic AIF-induced chromatin degradation (an indicator of caspa

45 factor (AIF) and co-localizes with apoptotic AIF.

46 icle formation and knock down of cathepsin B-AIF significantly reduced neratinib lethality.

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

48 Blocking AIF translocation resulted in a decreased apoptosis, sug

49 ings indicate that 16E6, but not 6E6, blocks AIF-mediated apoptosis, and that AIF may represent a nov

50 ments revealed that XIAP interacts with both AIF forms.

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

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

53 n the mitochondrial (cytosolic cytochrome C, AIF, Mcl-1, Bcl-2, Bcl-xl, Bax, Bad, and p-Bad) and ER s

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

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

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

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

58 Consequently, AIF deficiency expanded neovascularization and diminishe

59 is an attractive alternative to conventional AIF measurement.

60 l modeling was performed using the corrected AIF.

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

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

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

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

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

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

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

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

69 is principle in a new method for determining AIF, as shown by using [(11)C]PBR28 as a representative

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

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

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

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

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

75 othelial cells in affected tissues expressed AIF-1.

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

77 and apoptotic) of apoptosis-inducing factor (AIF) and co-localizes with apoptotic AIF.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

97 echanism by which apoptosis-inducing factor (AIF) regulates CI biogenesis by tracking the AI profile

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

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

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

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

102 rome c (CytC) and apoptosis-inducing factor (AIF) through upregulation of Bax expression and downregu

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

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

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

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

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

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

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

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

111 Apoptosis Inducing Factor (AIF), a mitochondrial proapoptotic protein, mediates cel

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

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

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

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

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

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

118 cytochrome C and apoptosis inducing factor (AIF), LC3B-positive neurons, and expression of LC3B, Bec

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

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

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

122 translocation of apoptosis-inducing factor (AIF).

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

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

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

126 translocation of apoptosis-inducing factor (AIF).

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

128 The allograft inflammatory factor (AIF) gene family consists of two identified paralogs - A

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

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

131 e analysis performed on selected samples for AIF correction.

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 A radiotracer arterial input function (AIF) is often essential for converting brain PET data in

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

141 rd representing the arterial input function (AIF).

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

143 reference standard (arterial input function [AIF]).

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

160 rinsic pathway involving caspase-independent AIF is also significant for chronic periodontitis.

161 ession in neurons prevented ischemia-induced AIF translocation.

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

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

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

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

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

167 Isolated AIF and AMID containing naturally incorporated FAD displ

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

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

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

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

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

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

174 labeled with carbon-11 (t(1/2) = 20.4 min), AIF is routinely determined with radio-HPLC of blood sam

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

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

177 glycolytic failure upstream of mitochondrial AIF release.

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

179 Moreover AIF-deficient PC3 cells exhibited substantial reduction

180 Moreover, AIF also regulated Bnip3 expression through mitochondria

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

182 forms of naturally folded recombinant murine AIF.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

197 translocation and intensified expression of AIF.

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

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

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

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

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

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

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

205 of very few known functional interactors of AIF.

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

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

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

209 PV, HPV6 (6E6), did not reduce the levels of AIF despite its interaction with AIF.

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

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

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

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

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

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

216 binding induced MG132-sensitive reduction of AIF expression in the presence of E6 derived from HPV16

217 hese data implicate Scythe as a regulator of AIF.

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

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

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

221 PAR in the nucleus triggering the release of AIF from the mitochondria.

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

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

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

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

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

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

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

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

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

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

232 ediated through the nuclear translocation of AIF.

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

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

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

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

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

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

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

240 In principle, AIF might be obtained by measuring the molar activity (A

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

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

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

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

245 well as mitochondrial intermembrane proteins AIF and Mia40.

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

247 athway involving autophagy and not requiring AIF.

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

249 ) were compared with the reference standard (AIF) using the absolute percentage difference between th

250 Subsequently, AIF translocates to the nucleus along with MIF causing c

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

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

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

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

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

256 6E6, blocks AIF-mediated apoptosis, and that AIF may represent a novel therapeutic target for HPV-ind

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

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

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

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

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

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

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

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

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

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

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

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

269 After the AIF reconstruction method was validated in healthy anima

270 ived using the motion-corrected IDIF and the AIF was (1.2% + 0.9%).

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

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

273 from the reference values obtained from the AIF.

274 his little-studied gene and its place in the AIF gene family.

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

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

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

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

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

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

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

282 ) values in gray matter calculated using the AIF and the IDIF.

283 We find that when the AIF-Mia40 translocation complex is disrupted, the part o

284 d motion-corrected dynamic sequence with the AIF based on the areas under the curves (AUCs).

285 Thus, AIF's effect on CI assembly is principally due to compro

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

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

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

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

290 When AIF analysis was applied to helical multidetector CT myo

291 sis by tracking the AI profile observed when AIF expression is impaired.

292 y recapitulates the AI profile observed when AIF is inhibited.

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

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

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

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

297 e levels of AIF despite its interaction with AIF.

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.