ライフサイエンスコーパス: FOXO3

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

2 action depended on the transcription factor Foxo3.

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

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

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

6 nin KD hepatocytes that failed to inactivate FoxO3.

7 lion neurons, both of which normally express Foxo3.

8 y were similarly repressed in the absence of FoxO3.

9 accompanied by increased phosphorylation of FOXO3.

10 by concomitant loss of transcription factor Foxo3.

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

12 neering them to express an activated form of FOXO3.

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

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

15 it Skp2 binds preferentially to deacetylated FOXO3.

16 s the stress-responsive transcription factor FoxO3.

17 direct downstream transcriptional target of FOXO3.

18 oncert to regulate the apoptotic function of FOXO3.

19 ed astrocyte differentiation and up-regulate FOXO3.

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

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

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

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 tiation into a range of vascular cell types. FOXO3-activated vascular cells exhibited delayed aging a

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

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

28 diated vascular protection and indicate that FOXO3 activation may provide a means for generating more

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

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

31 Here, we report that FoxO1, but not FoxO3, activity is essential for reciprocal regulation o

32 Foxo3 acts as an important central regulator that integr

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

50 nteract with the DNA-binding domain (DBD) of FOXO3 and modulate the FOXO3 transcriptional program in

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

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

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

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

55 there is also a positive correlation between FOXO3 and PERK expression at the protein and RNA levels

56 nd, we exploit this adaptive response of low FOXO3 and PERK expression, and high PERK activity in dru

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

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

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

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

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

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

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

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

65 repressed the expression of forkhead box O3 (FOXO3), and FOXO3 negatively regulated pathogenic T(h)17

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

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

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

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

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

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

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

73 y modulating genes such as mtor, insr, ampk, foxo3, and polg.

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

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

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

77 ll) and foxo whose orthologues NR2E1/TLX and FOXO3 are transcription factors implicated in human neur

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

79 Mechanistically, we have identified FOXO3 as a key downstream target of METTL3, with m(6) A

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

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

82 ypoxic tumor microenvironment and identifies FOXO3 as an important target of m(6) A modification in t

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

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

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

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

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

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

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

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

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

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

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

94 ding, we show that ectopic overexpression of FOXO3 can reduce the sensitivity of the resistant cells

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

96 Mechanistically, constitutively active FOXO3 conferred cytoprotection by transcriptionally down

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

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

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

100 ode of interaction between compounds and the FOXO3-DBD was assessed via NMR spectroscopy and docking

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

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

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

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

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

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

107 Consequently, Foxo3-deficient mice exhibited reduced susceptibility to

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

123 When tested in a therapeutic context, FOXO3-enhanced vascular cells promoted vascular regenera

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

125 f Foxo3 in mice that deletes the full-length Foxo3 except isoform2, a close ortholog of the human FOX

126 Consistently, we find that FOXO3 expression is attenuated in the drug-resistant MCF

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

128 g balanced hematopoietic output by buffering FOXO3 expression.

129 ogenicity, which was associated with reduced Foxo3 expression.

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

131 We analyzed FOXO3/FKHRL1 expression and subcellular localization in

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

133 xpression of the repressor foxo3, to prevent Foxo3 from binding to and repressing the vegfa promoter.

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

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 rminal truncated mutation of the full-length FOXO3 However, the biological function of FOXO3 isoform2

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 odulate the physiologic program activated by FOXO3 in cancer cells.

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

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

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

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

148 tudy, we established a conditional allele of Foxo3 in mice that deletes the full-length Foxo3 except

149 Silencing Foxo3 in mouse TADCs was also associated with diminished

150 Recent studies show the involvement of Foxo3 in osteoclastogenesis and rheumatoid arthritis, wh

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

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

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

156 7 (SIRT1 and SIRT7) are able to deacetylate FOXO3 in vitro and in vivo, and that lipopolysaccharide

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

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

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

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

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

162 Instead, FOXO3 induced phosphorylation of its binding partner ATM

163 whereas silencing PLIN2 or overexpression of FOXO3 inhibited proliferation.

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

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

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

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

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

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

170 Foxo3 is a critical repressed downstream effector that i

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

172 Thus, FOXO3 is a promising candidate target for immunotherapie

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

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

175 FOXO3 is an evolutionarily conserved transcription facto

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

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

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

179 FOXO3 is essential for DNA damage-induced apoptosis and

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

181 In consequence, FOXO3 is often downregulated as an adaptive response in

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

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

184 Foxo3 is required to maintain the ovarian reserve in mic

185 frequently inactivated in human cancers, and FOXO3 is the second most replicated gene associated with

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

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

188 Mechanistically, Foxo3 isoform2 enhances the expression of type I IFN res

189 th FOXO3 However, the biological function of FOXO3 isoform2 is unclear.

190 Expression of Foxo3 isoform2 specifically in macrophage/osteoclast lin

191 edge, the first known biological function of Foxo3 isoform2 that acts as a novel osteoclastic inhibit

192 Several databases document FOXO3 isoform2, an N-terminal truncated mutation of the

193 cept isoform2, a close ortholog of the human FOXO3 isoform2.

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

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

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

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

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

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

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

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

202 l samples furthermore showed that METTL3 and FOXO3 levels are tightly correlated in HCC patients.

203 which prompted us to further investigate the FOXO3 locus.

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

205 Foxo3 loss, combined with exposure to the DNA methylatio

206 NPCs and that this is exacerbated following FoxO3 loss.

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

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

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

210 -1, Atg9A, Atg4B, and Bnip3, suggesting that FoxO3 may function to maintain components of the autopha

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

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

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

214 r findings provide mechanistic insights into FOXO3-mediated vascular protection and indicate that FOX

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

216 t of METTL3, with m(6) A modification of the FOXO3 mRNA 3'-untranslated region increasing its stabili

217 by abolishing the identified METTL3-mediated FOXO3 mRNA stabilization, and overexpression of FOXO3 re

218 A FOXO3 mutant insensitive to inactivation by survival kin

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

220 e expression of forkhead box O3 (FOXO3), and FOXO3 negatively regulated pathogenic T(h)17 cell respon

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

222 on of atrogenes, upstream regulators (FOXO1, FOXO3, NFKB1A), key components of the ubiquitin proteaso

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

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

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

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

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

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

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

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

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

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

233 Basal Akt and FOXO3 phosphorylation was normal.

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

235 this network mediated by RBP-J/NFATc1-miR182-FoxO3/PKR (previously identified miR182 targets) towards

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

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

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

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

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

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

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

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

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

245 The tumour suppressive transcription factor FOXO3 promotes cell cycle arrest, senescence and cell de

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

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

248 Increased FoxO3 protein abundance leads to alterations in tubular

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

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

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

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

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

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

255 TFs) (STAT1, IRF7, SPI1, STAT4, IRF1, HIF1A, FOXO3, REL, NFAT5, HIC1, and IRF4) at 3 hours and a set

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

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

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

259 O3 mRNA stabilization, and overexpression of FOXO3 restores m(6) A-dependent sorafenib sensitivity.

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

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

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

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

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

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

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

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

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

269 ce all three phenotypes, of which five (near FOXO3, SLC4A7, LINC02513, ZW10, and FGD6) have not been

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

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

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

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

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

275 S9 and its oxalate salt S9OX interfere with FOXO3 target promoter binding, gene transcription and mo

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

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

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

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

280 irectly inhibits expression of the repressor foxo3, to prevent Foxo3 from binding to and repressing t

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

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

283 AMPK nuclear signaling pathway converging on FoxO3 transcription factor.

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

285 nding domain (DBD) of FOXO3 and modulate the FOXO3 transcriptional program in human cells.

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

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

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

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

290 triggering-factor, and transcription factor FOXO3 was a critical mediator for apoptotic EV-induced T

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

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

293 FOXO3 was identified as a negative regulator of Irf7 tra

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

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

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

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

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

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

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