ライフサイエンスコーパス: FOXO3

1 f forkhead family of transcription factor 3 (FoxO3).

2 und that E2F1 forms a complex with FOXO1 and FOXO3.

3 nin KD hepatocytes that failed to inactivate FoxO3.

4 lion neurons, both of which normally express Foxo3.

5 y were similarly repressed in the absence of FoxO3.

6 accompanied by increased phosphorylation of FOXO3.

7 by concomitant loss of transcription factor Foxo3.

8 the apteronotid homologs of FoxP2, Otx1, and FoxO3.

9 tified the Irf7 gene as a critical target of FOXO3.

10 ncomitant down-regulation of p21, Foxo1, and Foxo3.

11 it Skp2 binds preferentially to deacetylated FOXO3.

12 nhibits nuclear localization and activity of FoxO3.

13 ubiquitin ligases by a constitutively active FoxO3.

14 oncert to regulate the apoptotic function of FOXO3.

15 ed astrocyte differentiation and up-regulate FOXO3.

16 action depended on the transcription factor Foxo3.

17 tor and is mediated through up-regulation of FOXO3.

18 ed phosphorylation of muscle STAT3, p38, and FOXO3.

19 amino acid sequences: FoxP2, 78%; Otx1, 54%; FoxO3, 71%.

20 r extent, on average: FoxP2, 89%; Otx1, 76%; FoxO3, 82%.

21 g HSCs by targeting the transcription factor FOXO3, a known aging associated gene.

22 nuclear accumulation of transcription factor FoxO3, a positive regulator of erythroid anti-oxidant ge

23 THP-1 monocytes induced a rapid increase of FOXO3 acetylation, partly by suppression of SIRT1 and SI

24 Conditional FOXO3 activated caspase-8 gene expression but did not ch

25 Taken together, our findings indicate that FoxO3 activation can both induce and maintain autophagic

26 , in kidneys with persistent UUO for 7 days, FoxO3 activation increases the abundance of mRNA and pro

27 everaging GWAS data, Lee et al. now identify FOXO3 activity as predictive of disease severity in Croh

28 Rapamycin treatment increased FoxO3 activity as well as LC3 and ULK1 expressions in ma

29 Targeted disruption of FoxO3 also resulted in downregulation of antioxidant gen

30 context, the Forkhead transcription factor, Foxo3, amplified GATA-1-mediated transcriptional activat

31 shown by the translocation of phosphorylated FoxO3 (an inactive form) from nucleus to cytoplasm and t

32 n the regulation of the transcription factor FOXO3, an important regulator of Mn-superoxide dismutase

33 cancer cells led to a PI3K-dependent loss of FOXO3 and a decrease in the negative regulator of lipid

34 miR-182 reduces the expression of Bcat2, Foxo3 and Adcy6 to regulate the hypertrophic response in

35 on of SIRT1 and SIRT7 and failed to induce p-FOXO3 and apoptosis in response to LPS.

36 through STAT3 and p38 for the activation of FOXO3 and atrogin, but does not directly regulate the su

37 and alcohol together caused loss of nuclear FOXO3 and decreased its transcriptional activity.

38 ession of Skp2 caused poly-ubiquitination of FOXO3 and degradation, whereas knockdown of Skp2 increas

39 Forkhead (FOX) transcription factors, FOXK2, FOXO3 and FOXJ3 in vivo.

40 Silencing FOXO3 and Foxo3 with siRNAs abrogated the ability of hum

41 MP) mice, TADCs expressed elevated levels of FOXO3 and Foxo3, respectively, which correlated with exp

42 te block of differentiation, indicating that Foxo3 and Foxo4, although dispensable for male fertility

43 s and observed a correlation between nuclear FOXO3 and high caspase-8 expression.

44 Knockdown studies confirmed that FoxO3 and its downstream target, PUMA, were critical for

45 Taken together, these data implicate Foxo3 and its transcriptional targets in outer hair cell

46 Taken together, FOXO3 and LDs might serve as new targets for therapeutic

47 phagy in VCP-IBM muscle, we examined the AKT/FOXO3 and mammalian target of rapamycin (mTOR) pathways.

48 a direct protein-protein interaction between FOXO3 and NF-kappaB RelA in tumor-associated DCs.

49 udy demonstrates a novel mechanism involving FOXO3 and NF-kappaB RelA that controls myeloid cell sign

50 FoxO3 is a p53 target gene, and suggest that FoxO3 and p53 are part of a regulatory transcriptional n

51 former phenomenon is related to DCA-induced Foxo3 and p53 expression, resulting in the overexpressio

52 Blood, Karube and colleagues have identified FOXO3 and PRDM1 (Blimp1) as tumor suppressor genes with

53 GABP also directly regulates Foxo3 and Pten and hence sustains HSC quiescence.

54 associated with increased levels of p21 and FOXO3 and reduced expression of survivin.

55 Overall, our data suggest that FoxO3 and Sirt6, two longevity genes, can reduce LDL-cho

56 dent activation of the transcription factors FOXO3 and TFEB, which enhanced lipid catabolism and Mtb

57 sive for generation of the apoptotic form of FOXO3 and the activity of SIRT1 and particularly SIRT7 r

58 se results suggest an essential link between FOXO3 and the ATM-Chk2-p53-mediated apoptotic programme

59 d lower SIRT1 and SIRT7 and readily formed p-FOXO3 and underwent apoptosis when similarly treated.

60 e different nuclear and cytosolic species of FOXO3 and used antiphosphoserine, acetyl-lysine, methyla

61 hways, including the MAPK-ERK1/2, Stat3, Akt/Foxo3, and CXCR4/GPCR, which are all known to positively

62 ith the loss of Forkheadbox group O (Foxo)1, Foxo3, and Foxo4 expression.

63 Combined muscle-specific deletion of FoxO1, FoxO3, and FoxO4 in MIGIRKO mice reversed increased auto

64 ple liver-specific knock-outs lacking FoxO1, FoxO3, and FoxO4 or the related protein FoxA2.

65 Combined deficiency of Foxo1, Foxo3, and Foxo4 resulted in a severe impairment of SSC

66 the circumstance, FOXO (Forkhead O) (FOXO1, FOXO3, and FOXO4) transcription factors activate the exp

67 of three members of the FoxO family: FoxO1, FoxO3, and FoxO4.

68 al regulators (forkhead box [FOX] F2, FOXO1, FOXO3, and hypoxia inducible factor [HIF]-1alpha) were m

69 caspase activation, nuclear translocation of FoxO3, and increased proapoptotic PUMA expression.

70 ctivation and phosphorylation levels of Akt, FoxO3, and ribosomal protein S6 were determined by Weste

71 sceptibility of cells, and the importance of FoxO3 appears to change during development.

72 cessary for p53-dependent cell cycle arrest, FoxO3 appears to modulate p53-dependent apoptosis.

73 p300, and the active chromatin structure of Foxo3 are disrupted along with a loss of Foxo3 expressio

74 In this article, we show that the levels of FOXO3 are significantly decreased in lungs of smokers an

75 eserve in mice, thus emphasizing the role of Foxo3 as a guardian of the ovarian follicle pool in mamm

76 and have identified the transcription factor FOXO3 as a negative regulator of the magnitude and effec

77 ived from lacritin-stimulated acetylation of FOXO3 as a novel ligand for ATG101 and coupling of stres

78 These results implicate FOXO3 as a suppressor of LAC carcinogenesis, a role freq

79 Here we identify both FoxO1 and FoxO3 as direct targets of miR-9 in hematopoietic cells

80 Thus, p8 RNAi increases FoxO3 association with bnip3 promoter, a known proautoph

81 ultiple changes including phosphorylation of FOXO3 at S-574, a novel c-Jun N-terminal kinase (JNK) si

82 azadC) induced rapid nuclear accumulation of FOXO3, ATM-dependent CREB phosphorylation, and caspase-8

83 This indicates that 5-azadC activates the FOXO3-ATM-CREB signaling pathway, which contributes to c

84 We find that FOXO3 binds NF-kappaB RelA in the cytosol, impacting bot

85 xercise-induced nuclear transcription factor FOXO3 binds to the CHCHD4 promoter and represses its exp

86 The synergistic increase in nuclear p53 and FOXO3 by exercise can facilitate their known interaction

87 Activation of FoxO3 by mutating phosphorylation sites to enhance its n

88 Deacetylation of FOXO3 by SIRT activation or SIRT1 or SIRT7 overexpressio

89 ata support the notion that deacetylation of FOXO3 by SIRT1 or SIRT2 facilitates Skp2-mediated FOXO3

90 that overexpression of constitutively active FOXO3 can increase ovarian reproductive capacity in mice

91 Here, we show that loss of Foxo3 causes a myeloproliferative syndrome with splenome

92 Our combined results show that loss of Foxo3 causes increased ROS accumulation in HPs.

93 but not either condition alone, inactivates FOXO3, causing a decrease in expression of its target ge

94 Interestingly, autophagic cells deficient in FoxO3 contain lower numbers of autophagic vesicles per c

95 stored upon deletion of the same sequence in FOXO3 containing the DNA binding domain.

96 To determine the scope of the GATA-1/Foxo3 cooperativity, and to develop functional insights,

97 mechanism regulating autophagy by acting as FoxO3 corepressor, which may be relevant for diseases as

98 of lysine residues, we investigated whether FOXO3 deacetylation by SIRT1 or SIRT2 facilitates FOXO3

99 Foxo3 deficiency also led to a decrease in SIRT6, reveal

100 tylate the FOXO3 transcription factor, since Foxo3 deficiency diminished the protective effect of SRT

101 easing the cell cycle inhibitor p27kip1, and Foxo3 deficiency in mice results in marked colonic epith

102 lentiviral-based overexpression of Eomes in Foxo3-deficient CD4(+) T cells restored both IFN-gamma a

103 Here, we show in Foxo3-deficient colonic epithelial cells a striking incr

104 Consequently, Foxo3-deficient mice exhibited reduced susceptibility to

105 tosol, impacting both proteins by preventing FOXO3 degradation and preventing NF-kappaB RelA nuclear

106 nhibitor treatment prevented sirtuin-induced FOXO3 degradation, indicating that this process is prote

107 stically, we found that AMPKalpha1 regulates FoxO3-dependent expression of both LC3 and ULK1, which a

108 However, functionally, FOXO3-dependent gene regulation is generally mediated no

109 histological techniques, we demonstrate that Foxo3-dependent hearing loss is not due to a loss of coc

110 e cancer cells into non-cancerous cells in a FOXO3-dependent manner, and may allow patients to overco

111 cting to enhance E2F1-induced apoptosis in a FOXO3-dependent manner.

112 osphorylation, and caspase-8 expression in a FOXO3-dependent manner.

113 Collectively, our findings show that a FoxO3-dependent metabolic programme supports redox balan

114 functional insights, we analyzed the GATA-1/Foxo3-dependent transcriptome in erythroid cells.

115 In contrast, silencing FOXO3 diminishes all these cellular events when ovarian/

116 present evidence that SCF-Skp2 ubiquitinates FOXO3 directly in vitro.

117 long been evidence that acetylation promotes FOXO3-driven apoptosis and recently a specific JNK (c-Ju

118 sis in distinct diseases that operates via a FOXO3-driven pathway modulating inflammatory responses.

119 it inflammatory responses in monocytes via a FOXO3-driven pathway, which through TGFbeta1 reduces pro

120 Thus, the Foxo3-Eomes pathway is central to achieve the complete s

121 p53, TA-p73, and p300 binding and Foxo3 expression decrease during liver regeneration, and

122 s and cell death, whereas increased FoxO1 or FoxO3 expression reduces reactive oxygen species and cel

123 Here, we have shown that Foxo3 expression was increased after T cell receptor eng

124 ogenicity, which was associated with reduced Foxo3 expression.

125 of Foxo3 are disrupted along with a loss of Foxo3 expression.

126 g balanced hematopoietic output by buffering FOXO3 expression.

127 in SIRT6, revealing the existence of LD and FOXO3 feedback regulation in colonic cells.

128 We analyzed FOXO3/FKHRL1 expression and subcellular localization in

129 ion levels of three key proteins (Akt, FOXO1/FOXO3 [FOXO1/3], and mammalian target of rapamycin [mTOR

130 cumulates, causing partial relocalization of FoxO3 from nucleus to cytoplasm with dampening of its tr

131 the mechanisms by which mutations that alter Foxo3 function induce malignancy.

132 These results demonstrate that FOXO3 functions as a protective factor preventing alcoho

133 mall cell lung cancer, here, we identify the FOXO3 gene as a novel target of deletion in human lung a

134 inding to a site in the second intron of the FoxO3 gene, a genomic region recently found to be associ

135 Hence, FoxO3 has a central role in the neuronal reprogramming s

136 inase)-dependent S574 phosphorylated form (p-FOXO3) has been shown to be specifically apoptotic.

137 w that mice lacking the transcription factor Foxo3 have adult onset hearing loss with the hallmark ch

138 transfer corrects the abnormal expansion of Foxo3(-/-) HPs in vivo.

139 Elevated ROS levels result in defective Foxo3(-/-) HSC cycling, among many other deficiencies.

140 We provide further evidence that Foxo3(-/-) HSPC are defective in DNA damage repair.

141 es and suppressed IFN-I signaling via an AKT/FOXO3/IFN regulatory factor 3/7 pathway.

142 We also report anti-Foxo3 immunofluorescence in adult human outer hair cells

143 Loss of FoxO1 and FoxO3 in cardiomyocytes results in a significant increas

144 identified Eomes as a direct target gene for Foxo3 in CD4(+) T cells and we have shown that lentivira

145 We find that p53 transactivates FoxO3 in cells by binding to a site in the second intron

146 in diverse biological processes, the role of FoxO3 in cigarette smoke (CS)-induced lung inflammation

147 ole for the canonical damage response factor Foxo3 in contributing to the maintenance of auditory syn

148 wed the presence of the HCV-specific form of FOXO3 in HCV-infected livers but not in normal liver or

149 Conversely, deleting FoxO3 in mice results in fewer numbers of autophagic cel

150 Silencing Foxo3 in mouse TADCs was also associated with diminished

151 polycomb targets, including the promoter of Foxo3 In patient-derived GBM stem cells, CRISPR/Cas9 del

152 An additional role for Foxo3 in preserving hearing is likely, as low frequency

153 mouse ovaries increased nuclear exclusion of Foxo3 in primordial oocytes.

154 We report that ablation of FOXO3 in T cells reduced apoptosis, increased the abunda

155 orylation that coincide with localization of FoxO3 in the nuclear compartment.

156 apoptosis, confirming a proapoptotic role of FoxO3 in the stressed liver.

157 7 (SIRT1 and SIRT7) are able to deacetylate FOXO3 in vitro and in vivo, and that lipopolysaccharide

158 onsive transcription factor forkhead box O3 (FoxO3) in mediating injury-induced proximal tubular auto

159 idence for posttranslational modification of FoxO3, including early (6 hours) deacetylation and depho

160 Furthermore, shRNA-mediated deletion of FoxO3 increased hepatocyte resistance to oxidative stres

161 ibroblasts, whereas knockout or knockdown of FoxO3 increased the reprogramming efficiency of adult-de

162 n SIRT1, we detected increased expression of FOXO3, indicating SIRT1 regulates FOXO3 protein levels i

163 Instead, FOXO3 induced phosphorylation of its binding partner ATM

164 whereas silencing PLIN2 or overexpression of FOXO3 inhibited proliferation.

165 poietic cells and find that up-regulation of FoxO3 inhibits miR-9-induced myelopoiesis.

166 The transcription factor Foxo3 integrates the cellular response to oxidative stre

167 ranslocation of FoxO3 into the nucleus where FoxO3 interacted with NF-kappaB and disrupted NF-kappaB

168 Here we show that FOXO3 interacts with the ATM-Chk2-p53 complex, augments

169 sine residues (K242, K259, K290 and K569) of FOXO3 into arginines to mimic deacetylated FOXO3 resulte

170 showed that CS induced the translocation of FoxO3 into the nucleus where FoxO3 interacted with NF-ka

171 iption and we have further demonstrated that FOXO3, IRF7 and IFN-I form a coherent feed-forward regul

172 Our data suggest that the FOXO3-IRF7 regulatory circuit represents a novel mechani

173 Foxo3 is a critical repressed downstream effector that i

174 Our findings indicate that FoxO3 is a p53 target gene, and suggest that FoxO3 and p

175 Thus, FOXO3 is a promising candidate target for immunotherapie

176 Although FoxO3 is a well-known transcription factor involved in d

177 We show that following UUO, FoxO3 is activated and displays nuclear expression in th

178 The combined data suggest that FOXO3 is activated by 5-azadC treatment and triggers exp

179 The forkhead box transcription factor FOXO3 is an important component of the antioxidant stres

180 ic transcription factor and tumor suppressor FOXO3 is an important mediator of apoptosis, but the mec

181 By 16 hours, nuclear FoxO3 is both phosphorylated and acetylated.

182 FOXO3 is essential for DNA damage-induced apoptosis and

183 While FoxO3 is not necessary for p53-dependent cell cycle arre

184 To test whether FOXO3 is protective for alcoholic liver injury, we fed a

185 Here we show that Foxo3 is required for auditory function after noise expo

186 Foxo3 is required to maintain the ovarian reserve in mic

187 Foxo3 is the most responsive gene among transcription fa

188 Forkhead box class O 3a (FOXO3) is a member of the FoxO transcription factor subf

189 eover, Forkhead box O3 transcription factor (FoxO3) is further found to be required for GAA-mediated

190 he forkhead family of transcription factors, FOXO3, is a negative regulator of a subset of antiviral

191 Moreover, Foxo3-knock-out (KO) inner hair cells do not display red

192 The gene expression profile of Foxo3-/- knockout ovaries appears older than that of wil

193 how that synaptic localization is altered in Foxo3-KO mice and Myo7a immunoreactivity is reduced.

194 OXO3 preferentially bound JNK1, and a mutant FOXO3 lacking four known acetylation sites (K242, 259, 2

195 , therefore, hypothesized that deficiency of FoxO3 leads to increased susceptibility to CS-induced lu

196 Here, we show that loss of FOXO3 leads to the accumulation of DNA damage in primiti

197 In parallel, LD-dependent loss of FOXO3 led to its dissociation from the promoter and decr

198 Genetic ablation of FoxO3 led to pulmonary emphysema and exaggerated inflamm

199 We also find that FoxO3 loss does not interact with p53 loss for tumor dev

200 The potential role of FOXO3 loss in LAC was also investigated.

201 Foxo3 loss, combined with exposure to the DNA methylatio

202 NPCs and that this is exacerbated following FoxO3 loss.

203 p53-deficient mice appears to be affected by FoxO3 loss.

204 h glucosamine-mediated inhibition of the Akt/FoxO3/mammalian target of rapamycin pathway.

205 Under these conditions FOXO3 may also have a role in regulating chromatin reten

206 -1, Atg9A, Atg4B, and Bnip3, suggesting that FoxO3 may function to maintain components of the autopha

207 These findings demonstrate that FOXO3 may play a critical role in mediating TADC-induced

208 nding protein (CREB), which was critical for FOXO3-mediated caspase-8 expression.

209 from nucleus to cytoplasm and the release of FoxO3-mediated cell cycle arrest, thus leading to increa

210 us, SIRT1 protects against emphysema through FOXO3-mediated reduction of cellular senescence, indepen

211 or alcoholic liver injury, we fed alcohol to FOXO3(-/-) mice.

212 A FOXO3 mutant insensitive to inactivation by survival kin

213 amage accrued as a result of elevated ROS in Foxo3(-/-) mutant HSPC is at least partially reversible.

214 the foundation for future studies to use the FOXO3-NF-kappaB RelA interaction as a target to enhance

215 Another 60.6% of these tumors had losses of FOXO3 not reaching the level of HD (hereafter referred t

216 stress in cardiomyocytes promotes FoxO1 and FoxO3 nuclear localization and target gene activation.

217 Low-dose metformin or SN-38 increases FOXO3 nuclear localization as well as the amount of DNA

218 Strikingly, acoustic stimulation promotes Foxo3 nuclear localization in vivo, implying a connectio

219 riptional activity, and p8 knockdown affects FoxO3 nuclear localization.

220 Mechanistically, GAA promotes FoxO3 nuclear translocation and binding to the SESN2 enh

221 Loss of MEK-ERK signaling causes FoxO3 nuclear translocation and transcriptional activati

222 as validated using macrophages isolated from Foxo3-null mice.

223 we show that p53 regulates the expression of FoxO3, one of the four mammalian FoxO genes, in response

224 Inhibition of xCT, GCLM, FoxO3, or Nanog blocks chemotherapy-induced enrichment o

225 Absent Foxo3, outer hair cells are lost throughout the middle a

226 p53 and TA-p73 bind a Foxo3 p53 response element (p53RE) and maintain active e

227 e H3 at lysine 14, and acetylated H4) at the Foxo3 p53RE was detected after partial hepatectomy in mi

228 e, interference of the prosurvival IGF-I/AKT/FOXO3 pathway by redox activation of the stress kinases

229 cific deletion of genes in the PTEN-PI3K-Akt-Foxo3 pathway exhibited premature activation of all dorm

230 Modulation of the FOXO3 pathway is a potential therapeutic approach for HC

231 Basal Akt and FOXO3 phosphorylation was normal.

232 ad box of the O class transcription class 3 (FoxO3) phosphorylation and inhibited total GSK3 activity

233 Forkhead transcription factor FOXO3 plays a critical role in suppressing tumor growth,

234 The transcription factor Foxo3 plays a crucial role in myeloid cell function but

235 These results suggest that FoxO3 plays a pivotal role in regulation of lung inflamm

236 cell cycle and epigenetic regulators (e.g., Foxo3, Plk1, Mycn, Dnmt1, Dnmt3b, and Tet3).

237 We found that SIRT1 and SIRT2 promote FOXO3 poly-ubiquitination and degradation.

238 by SIRT1 or SIRT2 facilitates Skp2-mediated FOXO3 poly-ubiquitination and proteasomal degradation.

239 ing (IEF) method to determine the pattern of FOXO3 posttranslational modifications (PTMs) induced by

240 We also found that acetylated FOXO3 preferentially bound JNK1, and a mutant FOXO3 lack

241 r of oxidative DNA damage, is compromised in Foxo3(-/-) primitive hematopoietic cells.

242 Ethanol suppressed arginine-methylation of FOXO3 promoting nuclear export and degradation of the JN

243 species scavengers or ectopic expression of FOXO3 protects MLL4(-/-) MLL-AF9 cells from DNA damage a

244 lls is responsible for the downregulation of FOXO3 protein levels in these cells.

245 ression of FOXO3, indicating SIRT1 regulates FOXO3 protein levels in vivo.

246 as knockdown of Skp2 increased the amount of FOXO3 protein.

247 cohol combine to modify a complex pattern of FOXO3 PTMs that contribute to pathogenesis.

248 Herein, we demonstrate that among the FoxO3-regulated genes in NPCs are a host of enzymes in c

249 scription factor M1) and negative (FoxO1 and FoxO3) regulators of cardiomyocyte proliferation prenata

250 GATA-1/Foxo3 repressed expression of Exosc8, a pivotal componen

251 DNA damage-induced apoptosis and conversely FOXO3 requires ATM, Chk2 and phosphorylated p53 isoforms

252 TADCs expressed elevated levels of FOXO3 and Foxo3, respectively, which correlated with expression of

253 f FOXO3 into arginines to mimic deacetylated FOXO3 resulted in enhanced Skp2 binding but with inhibit

254 expression reduces the apoptotic function of FoxO3, resulting in increased hepatocyte survival.

255 nse and antioxidant genes, and deficiency of FoxO3 results in development of chronic obstructive pulm

256 the metabolic circuit observed upon loss of FoxO3 revealed a drop in glutaminolysis and filling of t

257 association between IGF-I concentration and FOXO3 (rs2153960, chromosome 6q21, P = 5.1 x 10(-7)), a

258 Collectively, our findings suggest that FOXO3 serves as a protector of HSC genomic stability and

259 tress-induced RPE necrosis by regulating the FoxO3/SESN2 pathway.

260 n suppressing EMT by modulating the Akt-MDM2-Foxo3 signaling axis.

261 -catenin-deficient livers, suggesting active FoxO3 signaling in response to DDC-induced liver injury

262 neous quantification of differently modified FOXO3 species allowed us to demonstrate how HCV and alco

263 In vivo, combined loss of FoxO1 and FoxO3 specifically in cardiomyocytes leads to delayed ce

264 h combined conditional deletion of FoxO1 and FoxO3 specifically in cardiomyocytes were subjected to I

265 escence staining revealed an intense nuclear FoxO3 staining in beta-catenin-deficient livers, suggest

266 ially block the autophagic flux suggest that FoxO3 stimulates the formation of autophagosomes to incr

267 te-specific combined deficiency of FoxO1 and FoxO3 subjected to myocardial infarction (MI) or acute i

268 Consistently, FoxO3 target genes p27 and Bim were significantly induce

269 n with bnip3 promoter, a known proautophagic FoxO3 target, resulting in higher bnip3 RNA and protein

270 te that GATA-1 utilizes the forkhead protein FoxO3 to activate select autophagy genes.

271 duced decrease in SOD2 and redistribution of FOXO3 to the cytosol.

272 ization of the forkhead transcription factor FoxO3 to the nucleus, thus inhibiting transcription of t

273 e recruited by forkhead transcription factor FoxO3 to the proximal promoter region of the Pcsk9 gene

274 ereby increasing binding of forkhead box O3 (FOXO3) to the ESR1 promoter.

275 in interaction was determined to be near the FOXO3 transactivation domain.

276 FoxO3 transcription factor was reported to activate auto

277 e to the ability of SIRT1 to deacetylate the FOXO3 transcription factor, since Foxo3 deficiency dimin

278 AMPK nuclear signaling pathway converging on FoxO3 transcription factor.

279 cell-specific deletion of both the Foxo1 and Foxo3 transcription factors (collectively called 'Foxo p

280 In agreement with the loss of Foxo3 transcriptional activation, a decrease in histone

281 her alcohol or HCV infection alone increased FOXO3 transcriptional activity and expression of target

282 P8 expression represses FoxO3 transcriptional activity, and p8 knockdown affects

283 s and decreased gonadotropin levels in aging FOXO3-transgenic mice compared with wild-type littermate

284 deacetylation by SIRT1 or SIRT2 facilitates FOXO3 ubiquitination and subsequent proteasomal degradat

285 enhanced Skp2 binding but with inhibition of FOXO3 ubiquitination; this suggests that some or all of

286 horylation, and thus, enhanced activation of FOXO3, up-regulation of MuRF1 and Atrogin-1, and progres

287 FOXO3 was activated by either HCV or alcohol alone but s

288 dependent and TA-p73-dependent activation of Foxo3 was also observed in mouse embryonic fibroblasts a

289 hesize that the anti-proliferative effect of FOXO3 was dependent on lowering LD density, thus decreas

290 Biallelic or homozygous deletion (HD) of FOXO3 was detected in 8 of 33 (24.2%) mostly early-stage

291 FOXO3 was identified as a negative regulator of Irf7 tra

292 In contrast, no HD of FOXO3 was observed in 19 lung squamous cell carcinoma.

293 t through regions occupied by both FOXK2 and FOXO3 where both factors play a regulatory role.

294 of a transcription factor, forkhead box O3 (FoxO3), which is implicated in aging, blocked iN cell co

295 nically, PS341 upregulated the expression of FOXO3, which inhibited the transcriptional activation of

296 Balancing ROS levels in HSC requires FOXO3, which is an essential transcription factor for HS

297 negative regulators of cytokine production: FOXO3, which is an inhibitory transcription factor, and

298 ocked the accelerated proteolysis induced by FoxO3, which is essential for atrophy.

299 a, as well as increased nuclear exclusion of FOXO3, which was suppressed by LA1-dependent activation

300 Silencing FOXO3 and Foxo3 with siRNAs abrogated the ability of human and mou