ライフサイエンスコーパス: FOXO1

1 transcription factor forkhead box class O1 (FOXO1).

2 forced by the expression of forkhead box O1 (FOXO1).

3 nstitutively active forkhead box protein O1 (FoxO1).

4 turation likely due to reduced activation of Foxo1.

5 phosphorylation of Ser(383) and Thr(649) in FOXO1.

6 coneogenesis via an interaction with hepatic Foxo1.

7 igated the mechanism by which ERK2 regulates FoxO1.

8 nucleus, reciprocal to the translocation of FoxO1.

9 agonism was promoter dependent and involved FOXO1.

10 rapamycin and its subsequent inactivation of FoxO1.

11 P9 expression and establish that it involves FOXO1.

12 oncogene and transcriptional target of PAX3-FOXO1.

13 In addition, the pro-apoptotic factors FoxO1/3 are overly degraded by acetylated Skp2, resultin

14 mice with muscle-specific triple knockout of FoxO1/3/4 and induced diabetes in these M-FoxO-TKO mice

15 At the molecular levels, hepatic Foxo1/3/4 deficiency triggered a significant increase in

16 et (HFC)-on wildtype (WT) and liver-specific Foxo1/3/4 triple knockout mice (LTKO).

17 four bona fide Akt substrates (TSC2, PRAS40, FOXO1/3a, and AS160) was reduced by ~50% in the absence

18 As a result, forkhead box O1 (FoxO1), a transcription factor that is negatively regula

19 f differentiation is determined, in part, by FOXO1, a transcription factor known to integrate extrins

20 FOXO1, a transcription factor, helps to determine this b

21 ngly, the protective effect of cardiomyocyte FOXO1 ablation in DbCM was abolished when KLF5 expressio

22 ndition, insulin fails to reduce the nuclear FOXO1 abundance and suppress gluconeogenic gene expressi

23 FOXO1 activates a stem cell molecular signature that is

24 In alveolar rhabdomyosarcoma, PAX3-FOXO1 activates SEs to induce the expression of other CR

25 tion of angiopoietin-2 (Ang2) in ECs through FOXO1 activation and triggering a positive feedback that

26 clusion, DOX exposure induces CDK2-dependent FOXO1 activation, resulting in cardiomyocyte apoptosis a

27 However, SD-Foxo1 actively repressed CD127 expression and failed to

28 tive oxygen species (ROS) or beta-catenin or FOXO1 activity abolished fibroblast p90RSK-mediated epit

29 Thus, numerous mechanisms maintain FOXO1 activity via AMPK signaling.

30 383) and Thr(649) complementarily stimulates FOXO1 activity.

31 trast, low nutrient and energy levels induce FOXO1 activity.

32 ng AKT activation and subsequently enhancing FOXO1 activity.

33 of the tumor driver and fusion protein PAX3-FOXO1, allowing downstream transcription of its oncogeni

34 orced expression of forkhead box protein O1 (FoxO1), an antagonist for activated Stat3, specifically

35 egulates the expression of the Rag activator Foxo1, an activity dependent on M303 in c-Myb's transact

36 by facilitating the nuclear translocation of FoxO1 and activation of key gluconeogenic genes, glucose

37 beta-cell dedifferentiation, as assessed by Foxo1 and Aldh1a3 immunohistochemistry.

38 -specific Cre recombinase deletion of floxed FOXO1 and compared the results to control littermates.

39 leading to Akt-mediated nuclear exclusion of FoxO1 and concomitant beta-catenin translocation to the

40 e longevity-associated transcription factors FOXO1 and DAF-16 in mammals and worms, respectively.

41 FOXO1 and ETV6 genes may represent novel regulators of s

42 ted proteasome activity and higher levels of FOXO1 and FOXO4 proteins.

43 that absence of BCAP hinders inactivation of FOXO1 and GSK3beta, which contributes to their enhanced

44 data with ChIP-seq/exo data for BCL6, SMRT, FOXO1 and H3K27ac identified direct targets of HDAC3 fun

45 of endogenous miR-486-5p activated PTEN and FoxO1 and induced cell death by upregulating proapoptoti

46 al expression of WT or constitutively active FoxO1 and insulin treatment are sufficient to regulate o

47 Hence, Fra-2 is a key upstream regulator of Foxo1 and Irf4 expression and influences proliferation a

48 ntiation were fully rescued by expression of Foxo1 and Irf4 in Fra-2-deficient pro-B cells.

49 DM1, in addition to a network coregulated by FOXO1 and IRF4.

50 nteraction of Aurora kinase A with both PAX3-FOXO1 and its effector MYCN, and reveal new opportunitie

51 Thus, FOXO1 and keratinocytes may be an important therapeutic

52 colysis enzyme); ATP levels; and cytoplasmic FoxO1 and Phospho-FoxO1, both of which control glycolyti

53 n the IGF1- or insulin-induced regulation of FOXO1 and present information useful both for therapeuti

54 targets the tumor suppressor genes PTEN and FoxO1 and regulates the GBM stem-like cells.

55 , which induces cytoplasmic translocation of FoxO1 and suppression of Notch signalling.

56 lar immune response, we report a gradient of FOXO1 and TCF7 expression, which functions to oppose TBE

57 Alternatively, decreased forkhead box O 1 (FOXO1) and increased K48 polyubiquitination also suggest

58 anscription factors forkhead box protein O1 (Foxo1) and Klf2 in DP thymocytes and the accumulation of

59 ulated transcription factor forkhead box O1 (FoxO1) and, accordingly, expression of FoxO1 is decrease

60 everal downstream targets, such as GSK3beta, FOXO1, and mTORC1, prior to NMDA-induced injury.

61 (beta-CATENIN, SMAD2/3, phospho-STAT3, P65, FOXO1, and phospho-ERK1/2) of key pathways commonly affe

62 t Dio2 is a direct transcriptional target of FoxO1, and the FoxO1-Dio2 axis governs TH-induced hypert

63 on of protein kinase B, nuclear exclusion of FOXO1, and the loss of FOXO1 transcription activity.

64 D-1 expression in vitro, responds to NFATc1, FoxO1, and/or NF-kappaB signaling pathways.

65 epressive cldn5-related transcription factor foxo1 are associated with stress resilience.

66 Mechanistically, we identified FOXO1 as a bona fide transcriptional repressor of HAS2.

67 ERK2, we identified the transcription factor FoxO1 as a potential mediator of ERK2-induced EMT, and t

68 Our results identify FOXO1 as a promising drug target for managing DOX-induce

69 rofiling identified the transcription factor FoxO1 as a SIRT1 target involved in transcriptional repr

70 ylation of the forkhead transcription factor FoxO1 at serine 256, which triggers its nuclear exclusio

71 of the transcription factor forkhead box O1 (FOXO1) at Ser-249, leading to transcription of its proap

72 Our results establish the Gfi1-Foxo1 axis and the transcriptional circuitry that active

73 identify the evolutionarily conserved SIRT1-FoxO1 axis as a regulator of resting CD8(+) memory T cel

74 es the expression of T-bet through Akt(S473)-FoxO1 axis, we further characterized the T-bet-deficient

75 FoxO1 binding is increased in genes regulated by pol II

76 occupying the Erag enhancer and antagonizing Foxo1 binding to a consensus forkhead site in this cis-r

77 AKT-mediated phosphorylation at serine 319, FOXO1 binds to IQGAP1, a hub for activation of the MAPK

78 the majority of their binding sites, whereby FOXO1 binds to multiple crucial self-renewal genes and i

79 This uncovered that FoxO1 binds to the promoters of 60% of cardiac-expressed

80 ChIP studies demonstrated that FoxO1 binds to three distinct sites located ~9 kb upstre

81 ombination therapy that interferes with PAX3-FOXO1 biology at different levels.

82 TP levels; and cytoplasmic FoxO1 and Phospho-FoxO1, both of which control glycolytic metabolism throu

83 orkhead box protein O1) deletion showed that FOXO1 bound directly on the KLF5 promoter and increased

84 the latter represents the majority (59%) of FoxO1-bound, pol II-regulated genes after pressure overl

85 Here, we report that FoxO1, but not FoxO3, activity is essential for reciproc

86 Phosphorylation of Foxo1 by Akt kinases at three distinct residues is well

87 oring RNA sequences bound to PGC-1alpha were Foxo1, Camk1delta, Per1, Klf15, Pln4, Cluh, Trpc5, Gfra1

88 cytoplasm and suggest that this function of FOXO1 can be harnessed to overcome chemoresistance in ca

89 Furthermore, we found that FOXO1 can bind to the promoter of TBX21 to inhibit its e

90 Our data demonstrate increases in FoxO1 chromatin binding during cardiac hypertrophic grow

91 To address this, we performed FoxO1 chromatin immunoprecipitation-deep sequencing in m

92 on pol II dynamics and gene expression, the FoxO1 chromatin immunoprecipitation-deep sequencing resu

93 es a dual conundrum: mechanistically, as the FOXO1 corepressor of glucokinase is unknown, and clinica

94 e report that SIN3A is the insulin-sensitive FOXO1 corepressor of glucokinase.

95 We provide evidence that SIRT6 is the FoxO1 deacetylase suppressed by mTORC2 and show an endog

96 pears to drive lipid catabolism by promoting FoxO1 deacetylation independently of AKT, and in a pathw

97 using a psoriasis-like mouse model in which Foxo1-deficient Tregs failed to protect mice from develo

98 ed upon Hdac3 loss and those up-regulated in Foxo1-deleted germinal center B cells, even though Foxo1

99 Diabetic mice with cardiomyocyte-specific FOXO1 deletion had lower cardiac KLF5 expression and wer

100 on stimulated by high glucose was blocked by FOXO1 deletion or FOXO1 knockdown.

101 FOXO1 deletion substantially blocked this increase.

102 tion and promotes lipogenesis by suppressing FOXO1-dependent activation of G6pase and inhibition of g

103 at non-cell-autonomous factors contribute to FoxO1-dependent effects on serpinB1 expression in the li

104 dent, early postinfection we report bimodal, FOXO1-dependent expression of the memory-essential trans

105 CD8 T cells, yet it is unclear whether these Foxo1-dependent functions are inherently coupled.

106 vates obesity-related insulin resistance via FoxO1-dependent hepatic gluconeogenesis.

107 mulating connective tissue healing through a FOXO1-dependent mechanism.

108 LPS effect on GFAT2 expression, suggesting a FoxO1-dependent mechanism.

109 that SD-Foxo1 was associated with a distinct Foxo1-dependent transcriptional profile, including genes

110 MAST4 in turn phosphorylated and inhibited FOXO1-dependent transcriptional repression of rhotekin 2

111 ffects are reversed by administering a small FOXO1-derived phospho-mimicking peptide inhibitor in vit

112 ect transcriptional target of FoxO1, and the FoxO1-Dio2 axis governs TH-induced hypertrophic growth o

113 ut mice, we unveil an essential role for the FoxO1-Dio2 axis in afterload-induced pathological cardia

114 ndings demonstrate a previously unrecognized FoxO1-Dio2 signaling axis in stress-induced cardiomyocyt

115 Inhibition of FoxO1 disrupts KSHV latency and induces viral lytic repl

116 e show that interactions within the PAX3 and FOXO1 domains are restricted to their respective TADs in

117 gulates FOXO1 protein expression and impairs FOXO1-driven gluconeogenic response.

118 as a novel metabolic regulator that promotes FOXO1-driven hepatic gluconeogenesis.

119 Thus, FOXO1 drives high levels of MMP9 expression in diabetic

120 the breadth of transcriptional regulation by FoxO1 during cardiac hypertrophy, information that is es

121 Thus, our studies uncover a link of FOXO1, ER stress and HIV infection that could be therape

122 is study, we show that an S209A phospho-null Foxo1 exhibited Akt-dependent nuclear trafficking in mou

123 downstream of Dock10 leads to an increase in FoxO1 expression and EMT.

124 hanism of cell death induced by loss of PAX3-FOXO1 expression and identified a novel pharmacologic co

125 Knockdown of FOXO4 but not FOXO1 expression decreased proteasome activity.

126 Conversely, decreased FOXO1 expression increases pERK1/2 in cancer cell lines

127 bition of the FoxO1 function or knockdown of FoxO1 expression led to an increase in the intracellular

128 robably from diminished transcription factor FOXO1 expression.

129 Thus, FoxK1/K2 are reciprocally regulated to FoxO1 following insulin stimulation and play a critical

130 ieved by preventing nuclear translocation of FoxO1 (Forkhead box protein O1) and beta-catenin, which

131 nd diabetic mice with cardiomyocyte-specific FOXO1 (Forkhead box protein O1) deletion showed that FOX

132 n kinase B) signaling and phosphorylation of FOXO1 (forkhead box protein O1) suppressing its transcri

133 xpression of atrogenes, upstream regulators (FOXO1, FOXO3, NFKB1A), key components of the ubiquitin p

134 Either chemical inhibition of the FoxO1 function or knockdown of FoxO1 expression led to a

135 Consistently, activation of FOXO1 function via inhibition of EGFR-AKT signaling prom

136 Strikingly, partial loss of Foxo1 function, but not restored survival fitness, recti

137 tions, such as unfavorable prognosis of PAX3-FOXO1 fusion in alveolar rhabdomyosarcoma.

138 nslocation that brings together the PAX3 and FOXO1 genes, the PAX3 promoter interacts ectopically wit

139 confocal fluorescence time-lapse imaging of FOXO1-GFP in adult isolated living muscle fibers maintai

140 o explore the effects of IGF1 and insulin on FOXO1-GFP nuclear efflux with and without pharmacologica

141 ERK inhibition restores FoxO1, gluconeogenic enzyme expression and glucose produ

142 ochondrial ROS, ERK activation and increases FoxO1, gluconeogenic enzyme expression and hepatocyte gl

143 Given that inactivation of FOXO1 has been reported in many types of human cancer, w

144 Genetic or pharmacological inhibition of FoxO1 impaired the LPS effect on GFAT2 expression, sugge

145 results unveil MAST4 as functional kinase of FOXO1 in a 27OHC AICD-driven, hormetic pathway providing

146 and phosphorylates the transcription factor FOXO1 in a glucose-dependent manner.

147 ying feed-forward loop among Trib3, Akt, and FoxO1 in Abeta-treated neurons induces both apoptosis an

148 More recently, mice lacking hepatic Foxo1 in addition to Akt1 and Akt2 (L-AktFoxo1TKO), all

149 ally be prevented by sustained expression of FoxO1 in beta-cells.

150 Depletion of PAX3-FOXO1 in fusion-positive (FP)-RMS cells induced intrinsi

151 importantly, overexpression of FOXO4 but not FOXO1 in HD NPCs dramatically enhanced proteasome activi

152 Expression of FOXO1 in human CD34(+) cells promotes a preleukemic stat

153 FOXO1 restored the pro-apoptotic function of FOXO1 in PCa.

154 The role of FOXO1 in regulating the function of Tregs was corroborat

155 Our works reveal a critical role of FoxO1 in suppressing KSHV lytic replication, which could

156 tumor suppressor role of AKT-phosphorylated FOXO1 in the cytoplasm and suggest that this function of

157 ogression, is a novel and major regulator of FOXO1 in the late phases of the cell cycle.

158 specific expression of constitutively active FoxO1 in transgenic mice induced an increase in hepatic

159 dant defense factor forkhead box protein O1 (FoxO1) in the KSHV life cycle.

160 n psoriatic Tregs, which subsequently caused FOXO1 inactivation by nuclear exclusion.

161 timulate binding of 14-3-3 proteins, causing FOXO1 inactivation.

162 iabetes-mediated activation of cardiomyocyte FOXO1 increases KLF5 expression, which stimulates NOX4 e

163 hat naive TCF7 (alias "Tcf-1") expression is FOXO1 independent, early postinfection we report bimodal

164 This stimulation is mediated by a FOXO1 induced TGFbeta1/CTGF axis.

165 dence that PLK1-dependent phosphorylation of FOXO1 induces its nuclear exclusion and negatively regul

166 ion, genetic and pharmacological ablation of FOXO1 inhibited the long-term proliferation and clonogen

167 Intriguingly, pharmacological FOXO1 inhibition also attenuated DOX-induced cardiac atr

168 over, activation of Src kinase signaling and FOXO1 inhibition decreased the expression of FOXO/BRD4 t

169 We report that, in resting T cells, FOXO1 inhibition impaired autophagy and induced endoplas

170 es revealed a mode of WNT signaling-mediated FOXO1 inhibition, potentially mediated through AKT.

171 r, N-acetyl-l-cysteine (NAC), attenuated the FoxO1 inhibition-induced intracellular ROS level and KSH

172 radical scavenger, led to a reduction in the FoxO1 inhibition-induced ROS level and, ultimately, the

173 cally suppressed HIV reactivation induced by FOXO1 inhibition.

174 cultured cardiomyocytes, treatment with the FOXO1 inhibitor AS1842856 or transfection with FOXO1-spe

175 We propose that FOXO1 inhibitors may have potential as cardioprotective

176 ional reduction of the transcription factors Foxo1, Irf4, Ikaros, and Aiolos in Fra-2-deficient B cel

177 Foxo1 is an essential transcription factor required for

178 generally considered as a tumor suppressor, FOXO1 is consistently upregulated in t(8;21) AML.

179 Our results show that FOXO1 is continuously required for all the phenotypic ch

180 x O1 (FoxO1) and, accordingly, expression of FoxO1 is decreased in the liver of trained and exosome-t

181 The DNA binding domain of FOXO1 is essential for these functions.

182 FoxO1 is involved in the pathogenesis of beta cell dysfu

183 FoxO1 is proteasomally degraded in SIRT1-deficient CD8(+

184 epatocytes from L-F1KO mice, suggesting that Foxo1 is required for E(2) action on the suppression of

185 Forkhead box protein O1 (FOXO1) is a transcription factor involved in various cel

186 Forkhead box protein O1 (FoxO1) is an insulin-sensitive transcription factor that

187 The forkhead box protein O1 (FOXO1) is considered to be a key tumor suppressor due to

188 yocyte hypertrophic growth is prevented with FoxO1 knockdown or deletion, which was accompanied by re

189 igh glucose was blocked by FOXO1 deletion or FOXO1 knockdown.

190 ized (OVX) female control and liver-specific Foxo1 knockout (L-F1KO) mice and sought to understand th

191 ss in wild-type and cardiomyocyte-restricted FoxO1 knockout mice, we unveil an essential role for the

192 wounds created in experimental K14.Cre (+) .Foxo1 (L/L) mice with lineage-specific Cre recombinase d

193 Mice lacking both the insulin receptor and FoxO1 (LIRFKO) exhibit reduced beta-cell mass compared w

194 cells with PI3K inhibitors or taxane causes FOXO1 localization in the nucleus, increased expression

195 using 2-photon live-cell imaging to monitor FoxO1 localization.

196 al advantages on cap cells via regulation of FOXO1 localization.

197 ikely the recruitment of corepressors to the Foxo1 locus by c-Myb.

198 racellular Ca(2+) and activation of AMPK and FOXO1, maintaining a low rate of cholangiocyte prolifera

199 dant defense factor forkhead box protein O1 (FoxO1) maintains KSHV latency by suppressing viral lytic

200 restoration of the pro-apoptotic activity of FOXO1 may be used as a new promising strategy for cancer

201 Together, our data suggest that FoxO1 may mediate cardiac hypertrophic growth via regula

202 FOXO1-mediated transcriptional repression of UBE3A was s

203 ins are major targets of insulin action, and FoxO1 mediates the effects of insulin on hepatic glucose

204 CK1 or ATM contributes to the suppression of FOXO1 nuclear efflux after IGF1.

205 Foxo1 nuclear efflux is promoted by AKT-mediated Foxo1 p

206 locks the IGF1- or insulin-induced effect on FOXO1 nuclear efflux, phosphatidylinositol 3-kinase inhi

207 ted activation of the PI3K/Akt/mTOR axis and FoxO1 nuclear exclusion in DCs, leading to decreased tra

208 This facilitates FoxO1 nuclear retention, enhances lipid uptake and lipol

209 AMPK inhibitors prevented Ghr-induced FOXO1 nuclear translocation and negative regulation of c

210 To assess the role of FoxO1 on pol II dynamics and gene expression, the FoxO1

211 el TAD that is likely to favour ectopic PAX3:FOXO1 oncogene activation in non-PAX3 territories.

212 of the genes encoding the downstream targets FOXO1 or ETV6 was sufficient to mimic these observations

213 tment did not elicit normal translocation of FoxO1 out of the nucleus.

214 OXO1 was shown to bind to the MMP9 promoter, FOXO1 overexpression increased MMP9 transcriptional acti

215 ], differentiation markers [Forkhead box O1 (FOXO1), Paired box 6, SRY box 9, NK6 Homeobox 1, NK6 Hom

216 indicate an uncoupling of the canonical Akt/FoxO1 pathway in HCV protein-expressing hepatocytes.

217 f TLR and BCR signaling pathways and the AKT/FOXO1 pathway in immune cells based on direct inhibition

218 abolism and highlight the relevance of SIRT1/FoxO1 pathway in obesity.

219 activation of the hypothalamic IR/IRS-2/AKT/FOXO1 pathway in response to insulin.

220 at the dysregulation of the protein kinase B-FOXO1 pathway may be a critical cause of Treg dysfunctio

221 rtin (POMC) neuronal activity, and the SIRT1/FoxO1 pathway regulates the inhibitory effect of MCH on

222 s in advanced PCa and support targeting PLK1-FOXO1 pathways as a novel approach for treating advanced

223 ntensity by mitigating the Kras/Erk and PI3K/Foxo1 pathways, and restricting the expression of PC tra

224 The crystal structure of a FOXO1 peptide in complex with 14-3-3 sigma at 2.3 angstr

225 rofile, exhibited by elevated phosphorylated-Foxo1, phosphorylated-Akt1, and decreased Bim-expression

226 its suppression of HAS2 transcription, with FOXO1 phosphorylation status maintained by operation of

227 However, the effect of Foxo1 phosphorylation within its DNA-binding domain at s

228 exhibited reduced Akt activity and decreased FOXO1 phosphorylation, a process known to promote transc

229 1 nuclear efflux is promoted by AKT-mediated Foxo1 phosphorylation, eliminating FOXO1's atrophy-promo

230 f hepatic glucose production (HGP), in which Foxo1 plays a central role in the regulation of gluconeo

231 These findings reveal that FoxO1 plays a critical role in keeping KSHV latency in c

232 Here we report that FoxO1 plays a critical role in promoting serpinB1 expres

233 estion, we examined the effects of different Foxo1 posttranslational modifications.

234 ransactivation of canonical target genes, SD-Foxo1 promoted IL-15-mediated CD8 T cell survival in vit

235 As a key regulator of T-cell quiescence, FOXO1 promotes latency and suppresses productive HIV inf

236 These results indicate that liver FoxO1 promotes serpinB1 expression in hepatic insulin re

237 f Cry1 in the mouse liver not only increases FOXO1 protein but also enhances hepatic gluconeogenesis.

238 Lack of Ddb1 downregulates FOXO1 protein expression and impairs FOXO1-driven glucon

239 knockout mice and their upstream regulator, FoxO1 protein levels are decreased via proteasome-depend

240 ols hepatic glucose production by regulating FoxO1 protein levels via proteasome-dependent degradatio

241 A most efficiently negatively affected PAX3-FOXO1 protein levels.

242 nistically, we discovered that DDB1 enhances FOXO1 protein stability via degrading the circadian prot

243 ntify drugs that alter the stability of PAX3-FOXO1 protein, the same drug library was screened and fu

244 A), AMP-activated protein kinase (AMPK), and FoxO1 proteins.

245 33b mimic or with a specific siRNA targeting FoxO1 recapitulates the metabolic effects observed in tr

246 ensitivity with increased phosphorylation of FOXO1, reduced expression of PEPCK, and increased glucok

247 N5L1 modulates post-translational control of FoxO1, regulates gluconeogenesis and controls metabolic

248 Akt-mediated phosphorylation of FOXO1 relieved its suppression of HAS2 transcription, wi

249 In this study, we show that increased FOXO1 represents a critical mechanism driving aberrant s

250 Conversely, FoxO1 responded to Abeta insult by binding to the Trib3

251 ocking the PLK1-dependant phosphorylation of FOXO1 restored the pro-apoptotic function of FOXO1 in PC

252 Moreover, deletion of Foxo1 restores the expression of T-bet and corrects the

253 (-8)): TEX41 (rs1006923; P = 5.3 x 10(-12)), FOXO1 (rs7331212; P = 2.2 x 10(-11)), C1orf21 (rs1930290

254 -mediated Foxo1 phosphorylation, eliminating FOXO1's atrophy-promoting effect.

255 s an additional AMPK phosphorylation site in FOXO1's N terminus, with Ser(22) phosphorylation prevent

256 s nuclear exclusion and negatively regulates FOXO1's transcriptional activity in prostate cancer (PCa

257 FOXO1's transcriptional activity is controlled by differ

258 nd Sell In contrast, an S209D phosphomimetic Foxo1 (SD-Foxo1) was largely excluded from the nucleus o

259 the PAX3 promoter interacts ectopically with FOXO1 sequences.

260 tion of AKT(ser473), ERK(thr202/tyr204), and FOXO1(ser256) as well as blunts AgRP gene transcription.

261 Genome-wide binding studies show that AE and FOXO1 share the majority of their binding sites, whereby

262 rotein Bim expression through regulating Akt-FoxO1 signaling and also attenuates H2O2-induced Bim act

263 pproaches to show that the sirtuin 1 (SIRT1)/FoxO1 signaling pathway in the hypothalamic arcuate nucl

264 ough ROS-mediated activation of beta-catenin/FOXO1 signaling pathway.

265 ptor (ER)alpha-phosphoinositide 3-kinase-Akt-Foxo1 signaling, which can be independent of insulin rec

266 XO1 inhibitor AS1842856 or transfection with FOXO1-specific siRNAs protected against DOX-induced apop

267 is a critical residue for the regulation of Foxo1 subcellular localization and for balancing CD8 T c

268 Here we generated a genome-wide map of FoxO1 superenhancers in chemically identified beta cells

269 with acute inactivation of the gene encoding FOXO1, T cells revert to a short-lived effector phenotyp

270 dy reveals a novel role for mTORC2-Akt(S473)-FoxO1-T-bet axis in suppressing the transcriptional sign

271 original 5'- and 3'- borders of the PAX3 and FOXO1 TADs, respectively, suggesting that TAD organisati

272 muscle RING finger 1 (MuRF1), a proatrophic FOXO1 target gene.

273 n treatment are sufficient to regulate other FoxO1 target genes (IGFBP-1 and PEPCK) but not serpinB1

274 ation of glucokinase without affecting other FOXO1 target genes and lowers glycemia without concurren

275 ls and augmented the expression of canonical Foxo1 target genes such as Il7r and Sell In contrast, an

276 Targeting of FOXO1 therefore provides a potential therapeutic strateg

277 s in synergy with metabolic stress-activated FOXO1 through formation of a complex.

278 e, caused by oxidative stress that activated FOXO1 to promote expression of Pnpla2/ATGL.

279 e AKT phosphorylates Thr(24) and Ser(256) in FOXO1 to stimulate binding of 14-3-3 proteins, causing F

280 nuclear exclusion of FOXO1, and the loss of FOXO1 transcription activity.

281 synthase and led to nuclear exclusion of the FOXO1 transcription factor, reducing expression of pro-i

282 icient T(reg) cells ameliorated disease in a Foxo1 transcription factor-dependent manner.

283 ing and may act in part through the ETV6 and FOXO1 transcription factors.

284 e-specific deletion of the forkhead box-O 1 (FOXO1) transcription factor, we demonstrate for the firs

285 aling pathways in a small motif to fine-tune FOXO1 transcriptional activity.

286 ct residues is well characterized to inhibit Foxo1 transcriptional activity.

287 e BBB via the modulation of forkhead box O1 (FoxO1) transcriptional activity and induces a tight junc

288 vitro, in part by inducing expression of the FOXO1 tumor suppressor gene.

289 deleted germinal center B cells, even though Foxo1 typically activates transcription.

290 Previously we demonstrated that FOXO1 was activated in wound healing but to higher level

291 RNA sequencing analysis revealed that SD-Foxo1 was associated with a distinct Foxo1-dependent tra

292 protein kinase B-mediated phosphorylation of FOXO1 was observed in psoriatic Tregs, which subsequentl

293 By chromatin immunoprecipitation FOXO1 was shown to bind to the MMP9 promoter, FOXO1 over

294 f the insulin-regulated transcription factor FoxO1 was somewhat reduced and insulin treatment did not

295 contrast, an S209D phosphomimetic Foxo1 (SD-Foxo1) was largely excluded from the nucleus of CD8 T ce

296 markers (DNA damage inducible transcript 3, FOXO1) were dysregulated in stressed EndoC-betaH1 cells,

297 and Rag 1/2, downstream targets of Irf4 and Foxo1, were also reduced in the absence of Fra-2.

298 ression of the oncogenic fusion protein PAX3-FOXO1, which is critical for tumorigenesis and cell surv

299 or 20% of disease associated loci, including FOXO1, which we confirm using CRISPR/Cas9.

300 proteasome system (ERK5), Tsc1/Tsc2 complex, FoxO1, wnt/beta-catenine signaling pathway.