ライフサイエンスコーパス: AIF

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

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

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

4 translocation of apoptosis-inducing factor (AIF).

5 translocation of apoptosis-inducing factor (AIF).

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

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

8 translocation of apoptosis-inducing factor (AIF).

9 l modeling was performed using the corrected AIF.

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

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

12 forms of naturally folded recombinant murine AIF.

13 athway involving autophagy and not requiring AIF.

14 hese data implicate Scythe as a regulator of AIF.

15 of very few known functional interactors of AIF.

16 ant displayed a more robust interaction with AIF.

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

18 translocation and intensified expression of AIF.

19 ediated through the nuclear translocation of AIF.

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

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

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

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

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

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

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

27 < 0.005), which was due to stabilization of AIF-1 isoform 2 mRNA.

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

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

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

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

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

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

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

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

36 AIF-1 significantly increased Jurkat T cell migration to

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

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

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

40 othelial cells in affected tissues expressed AIF-1.

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

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

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

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

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

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

47 Thus, Aif, a ubiquitous protein, serves a lineage-specific non

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

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

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

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

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

53 Moreover, AIF also regulated Bnip3 expression through mitochondria

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

55 When AIF analysis was applied to helical multidetector CT myo

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

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

58 Isolated AIF and AMID containing naturally incorporated FAD displ

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

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

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

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

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

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

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

66 well as mitochondrial intermembrane proteins AIF and Mia40.

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

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

69 Scythe physically interacts with AIF and regulates its stability.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

101 dominant mutations activate both the calpain-Aif cell death pathway and ER-stress responses that toge

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

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

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

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

106 e analysis performed on selected samples for AIF correction.

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

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

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

110 Consequently, AIF deficiency expanded neovascularization and diminishe

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

112 Aif-deficiency in T cells led to decreased peripheral T

113 In contrast, Aif-deficient B cells developed and functioned normally.

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

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

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

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

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

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

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

121 Moreover AIF-deficient PC3 cells exhibited substantial reduction

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

123 ression rescued homeostatic proliferation of Aif-deficient T cells.

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

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

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

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

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

129 ing oxidoreductase activity-deficient mutant Aif does not.

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

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

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

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

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

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

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

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

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

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

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

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

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

143 ments revealed that XIAP interacts with both AIF forms.

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

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

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

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

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

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

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

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

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

153 AIF has been known to have both apoptotic and metabolic

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

155 We report that aif-hypomorphic harlequin (Hq) mice show thymic hypocell

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

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

158 Here, we report that partial knockdown of Aif in mice recapitulates many features of CKD, in assoc

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

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

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

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

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

164 we describe the consequences of inactivating Aif in the early mouse embryo.

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

166 n of calpains and apoptosis-inducing factor (Aif) in dying photoreceptors.

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

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

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

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

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

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

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

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

175 n to its role in postmitotic neuron survival Aif is also necessary for cerebellar development, we ana

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

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

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

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

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

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

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

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

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

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

186 Apoptosis-inducing factor (Aif) is a mitochondrial flavoprotein that regulates cell

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

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

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

190 When diabetes was superimposed onto Aif knockdown, there were extensive changes in mitochond

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

207 Because of this cell death, Aif null embryos fail to increase significantly in size

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

209 Additional analysis revealed that Aif-null Purkinje cell precursors prematurely entered S-

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

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

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

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

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

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

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

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

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

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

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

221 After the AIF reconstruction method was validated in healthy anima

222 ng wild-type or DNA-binding-deficient mutant Aif rectify the thymic defect, but a transgene encoding

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

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

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

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

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

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

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

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

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

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

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

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

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

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

237 glycolytic failure upstream of mitochondrial AIF release.

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

239 deltaATPase) failed to prevent mitochondrial AIF release.

240 ondrial membrane permeability transition and AIF release.

241 gnificantly reduced VDAC oligomerization and AIF release.

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

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

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

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

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

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

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

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

250 Our results indicate that the loss of Aif results in cell cycle abnormalities in a neuron-spec

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

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

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

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

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

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

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

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

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

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

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

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

263 AIF translocates to the host cell nucleus, implying that

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

265 Blocking AIF translocation resulted in a decreased apoptosis, sug

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

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

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

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

270 ession in neurons prevented ischemia-induced AIF translocation.

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

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

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

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

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

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

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

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

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

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

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

282 ar development, we analyzed embryos in which Aif was deleted in the prospective midbrain and cerebell

283 Mice in which Aif was deleted later in embryogenesis using a nestin pr

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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