ライフサイエンスコーパス: AIF

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

2 translocation of apoptosis-inducing factor (AIF).

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

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

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

6 rd representing the arterial input function (AIF).

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

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

9 l modeling was performed using the corrected AIF.

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

11 e levels of AIF despite its interaction with AIF.

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

13 forms of naturally folded recombinant murine AIF.

14 athway involving autophagy and not requiring AIF.

15 hese data implicate Scythe as a regulator of AIF.

16 of very few known functional interactors of AIF.

17 ant displayed a more robust interaction with AIF.

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

19 from the reference values obtained from the AIF.

20 translocation and intensified expression of AIF.

21 n the area - we unveil a 3D geometry for the AIFS.

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

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

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

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

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

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

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

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

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

31 AIF-1 significantly increased Jurkat T cell migration to

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

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

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

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

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

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

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

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

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

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

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

43 Moreover, AIF also regulated Bnip3 expression through mitochondria

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

45 When AIF analysis was applied to helical multidetector CT myo

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

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

48 Isolated AIF and AMID containing naturally incorporated FAD displ

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

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

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

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

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

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

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

56 well as mitochondrial intermembrane proteins AIF and Mia40.

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

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

59 Scythe physically interacts with AIF and regulates its stability.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

97 e analysis performed on selected samples for AIF correction.

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

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

100 Consequently, AIF deficiency expanded neovascularization and diminishe

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

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

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

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

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

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

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

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

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

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

111 Moreover AIF-deficient PC3 cells exhibited substantial reduction

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

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

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

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

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

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

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

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

120 ing oxidoreductase activity-deficient mutant Aif does not.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

135 ments revealed that XIAP interacts with both AIF forms.

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

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

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

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

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

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

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

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

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

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

146 AIF has been known to have both apoptotic and metabolic

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

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

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

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

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

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

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

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

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

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

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

158 initial-stage, the Al-Idrissi Fault System (AIFS), in the Alboran Sea.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

177 al and instrumental events supports that the AIFS is currently growing through propagation and linkag

178 the fault segmentation and demonstrate that AIFS is the source of the 2016 events.

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

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

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

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

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

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

185 AIF knockdown reduced STS-induced apoptosis in both of 1

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

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

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

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

190 6E6, blocks AIF-mediated apoptosis, and that AIF may represent a novel therapeutic target for HPV-ind

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

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

193 is an attractive alternative to conventional AIF measurement.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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 Thus, the AIFS provides a unique model of the inception and growth

222 After the AIF reconstruction method was validated in healthy anima

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

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

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

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

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

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

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

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

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

232 ondrial membrane permeability transition and AIF release.

233 gnificantly reduced VDAC oligomerization and AIF release.

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

235 glycolytic failure upstream of mitochondrial AIF release.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

257 AIF translocates to the host cell nucleus, implying that

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

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

260 Blocking AIF translocation resulted in a decreased apoptosis, sug

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

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

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

264 ession in neurons prevented ischemia-induced AIF translocation.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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).