ライフサイエンスコーパス: FOXO1

1 anscription factor, forkhead box protein O1 (FoxO1).

2 ranscription factor Forkhead box protein O1 (FoxO1).

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

4 nstitutively active forkhead box protein O1 (FoxO1).

5 P9 expression and establish that it involves FOXO1.

6 aberrantly induced the transcription factor Foxo1.

7 rly reduced binding of RNA polymerase II and FoxO1.

8 tor, GLUT4, AS160, ribosomal protein S6, and FOXO1.

9 neogenic genes, including G6Pase, PEPCK, and FOXO1.

10 e RMS in vitro, which resembled loss of PAX3-FOXO1.

11 in signaling to stimulate phosphorylation of FOXO1.

12 essed expression of the transcription factor Foxo1.

13 denoviral infection of constitutively active FOXO1.

14 action required PI3K and Akt, which suppress FoxO1.

15 s of the PI3K/Akt pathway acting upstream of Foxo1.

16 rapamycin and its subsequent inactivation of FoxO1.

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

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

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

20 s for knock-in alleles encoding deacetylated FoxO1 (6KR).

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

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

23 Upon FOXO1 ablation or induction of PI3K activity, GCs lost t

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

25 FOXO1 activates a stem cell molecular signature that is

26 bition, we characterized a mechanism linking FOXO1 activation and HRK induction that involves caspase

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

28 ng as an agonist, promoting high p-Tie2, low FOXO1 activation, and no leakage.

29 led to p-Tie2 suppression, forkhead box O1 (FOXO1) activation, increased ANG2 expression, and vessel

30 est and apoptosis, indicating that increased FOXO1 activity is toxic to these DLBCL cells.

31 nesis because they suggest that constitutive FOXO1 activity might be required for the oncogenic activ

32 es CHD4 as an epigenetic coregulator of PAX3-FOXO1 activity, providing rational evidence for CHD4 as

33 modeler, acts as crucial coregulator of PAX3-FOXO1 activity.

34 We find that FOXO1 acts as a gatekeeper of endothelial quiescence, wh

35 These results suggest that Foxo1 acts as a repressor of albumin expression.

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

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

38 eRMS), HO-1 expression was induced by Pax3/7-FoxO1, an aRMS hallmark oncogene, followed by a drop in

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

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

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

42 ion of histone H3 Lys-27 accompanies loss of FoxO1 and FoxA1/A2 binding.

43 possibly entails cooperative binding because FoxO1 and FoxA1/A2 facilitate one another's binding to I

44 Interdependent binding of FoxO1 and FoxA1/A2 possibly entails cooperative binding

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

46 little is known about how insulin regulates FOXO1 and how FOXO1 may contribute to insulin resistance

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 Thus, FOXO1 and keratinocytes may be an important therapeutic

50 Immature NK cells expressed abundant Foxo1 and little Tbx21 relative to mature NK cells, but

51 e-induced insulin secretion, are depleted of Foxo1 and MafA, and include a Neurogenin3-positive subse

52 h induced nucleocytoplasmic translocation of FOXO1 and PDX1 and led to the differentiation of human p

53 ity in autoimmune diseases via inhibition of Foxo1 and present promising therapeutic targets.

54 ork, we have defined the interactome of PAX3-FOXO1 and screened 60 candidate interactors using siRNA-

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 target genes that required co-regulation by FOXO1 and TH.

58 , and we compared these results with hepatic FOXO1 and THRB1 (TRbeta1) ChIP-Seq data.

59 Interestingly, both FOXO1 and thyroid hormone (TH) have similar effects on c

60 HIPPO signaling pathways and inactivation of FOXO1 and YAP.

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

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

63 gnaling inactivates the transcription factor FOXO1, and a Foxo1 genetic deletion allowed for generati

64 e characterized by high CD25, CTLA4, pSTAT5, FoxO1, and GATA1 expression without a corresponding incr

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

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

67 ss-catenin, AKT, p42/44 MAPK, GAB2, GSK-3ss, FOXO1, and YAP.

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

69 ctase inhibitors may operate through a novel Foxo1-angiopoietin-2 mechanism to suppress de novo produ

70 lular abundance and consequently activity of FOXO1 are halved in T2D.

71 e exact transient expression pattern as PAX3-FOXO1 are specific to rhabdomyosarcoma cells.

72 This finding, which established FoxO1 as a "pioneer" factor, suggested a model whereby F

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

74 Our findings identify FOXO1 as a critical rheostat of vascular expansion and d

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

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

77 PLK1 interacted with and phosphorylated PAX3-FOXO1 at the novel site S503, leading to protein stabili

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

79 e preclinical studies validate the PLK1-PAX3-FOXO1 axis as a rational target to treat aRMS.

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

81 ore compelling candidate genes (for example, FOXO1, AZI2) often situated several megabases away; and

82 sed, and an attenuated decrease in % nuclear FoxO1+ beta cells was evident in response to glucose gav

83 ells and a significant decrease in % nuclear FoxO1+ beta-cells compared with corresponding vehicle-tr

84 lin showed significantly decreased % nuclear FoxO1+ beta-cells suggesting direct effects.

85 ic increased EC migration, increased Mdm2 to FoxO1 binding (+55%), and decreased FoxO1-dependent gene

86 te that 4 h after 10% FBS-containing medium, FOXO1 binding markedly decreases, and the DIO2 promoter

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

88 We show that DNA damage led to the loss of FOXO1 binding to the enhancer region of the RAG1/2 locus

89 e, involving the ATM-dependent regulation of FOXO1 binding to the Erag enhancer region.

90 also demonstrate that shRNA-mediated loss of FoxO1 binding to the IGFBP1 and G6Pase promoters in HepG

91 FoxO1 binds to insulin response elements located in the

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

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

94 CRY1 promotes degradation of nuclear FOXO1 by promoting its binding to the ubiquitin E3 ligas

95 known about the regulation of MTORC2-AKT or FOXO1 by TH.

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

97 ough this is likely independent of the NR4A3/FOXO1/CCR7 axis in the regulation of DC migration.

98 nd rapid proteasomal degradation of the PAX3-FOXO1 chimeric oncoprotein.

99 "pioneer" factor, suggested a model whereby FoxO1 chromatin remodeling at regulatory targets facilit

100 gion of the RAG1/2 locus (Erag) and provoked FOXO1 cleavage.

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

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

103 We also report that nuclear localization of FOXO1 correlated with PTEN mutational status irrespectiv

104 he gene expression signature associated with FoxO1 deacetylation differs from wild type by only appro

105 Two studies in this issue report that Foxo1 deficiency causes an almost complete loss of dark

106 Using mixed bone marrow chimeras and Foxo1-deficient mice, we demonstrate that this control i

107 ulates gluconeogenesis through CRY1-mediated FOXO1 degradation and that dysregulation of hepatic SREB

108 nd decreases hepatic gluconeogenesis through FOXO1 degradation, at least, at specific circadian time

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

110 FOXO1 deletion substantially blocked this increase.

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

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

113 Mdm2 to FoxO1 binding (+55%), and decreased FoxO1-dependent gene expression compared with ECs overex

114 rentiation was associated with repression of Foxo1-dependent gene transcription, concomitant with red

115 Tfh cell contingency that is completed in a FOXO1-dependent manner.

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

117 206 with R406 and found markedly synergistic FOXO1-dependent toxicity.

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

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

120 Finally, we found that FoxO1 directly targets and negatively regulates tyrosine

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

122 fic insulin receptor knockout (LIRKO) and IR/FoxO1 double knockout (LIRFKO) mice.

123 d initiates a positive feedback loop wherein FOXO1-driven ANG2 expression promotes vascular remodelin

124 o-AKT and phospho-FOXO1 levels and triggered FOXO1-driven gene expression.

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

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

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

128 ink between at least some ARMSs and the PAX3-FOXO1-expressing myogenic cells and demonstrate that fus

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

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

131 In primary DLBCLs, FOXO1 expression was present in 80% of tumors, correlate

132 gene transcription, concomitant with reduced Foxo1 expression, cytoplasmic localization and enhanced

133 robably from diminished transcription factor FOXO1 expression.

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

135 ownstream through protein kinase B (AKT) and FOXO1 (forkhead box protein O1) to drive synergistic exp

136 at the molecular level, we demonstrate that Foxo1 forms a complex with RORgammat via its DNA binding

137 Combined muscle-specific deletion of FoxO1, FoxO3, and FoxO4 in MIGIRKO mice reversed increas

138 malian target of rapamycin and FOXO proteins FOXO1, FOXO3A, and FOXO4 and decreased peroxisome prolif

139 osphorylation and subsequent preservation of Foxo1 function are critical.

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

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

142 issue tumor, which exists in oncoprotein PAX-FOXO1 fusion positive and fusion negative subtypes, with

143 lar interest in targeting the oncogenic PAX3-FOXO1 fusion transcription factor, which induces alveola

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

145 ivates the transcription factor FOXO1, and a Foxo1 genetic deletion allowed for generation of Tfh cel

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

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

148 The transcription factor FOXO1 has been shown to regulate CCR7 expression.

149 Islets expressing 6KR mutant FoxO1 have enhanced insulin secretion in vivo and ex viv

150 eatosis specifically highlighted activity of FOXO1&HNF4alpha on CPT2, the lipid droplet and ER-lipid-

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

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

153 We integrate insulin control of FOXO1 in a network-wide mathematical model of insulin si

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

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

156 Ablation of FOXO1 in AgRP neurons of mice results in reduced food in

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

158 Collectively, these results suggest that FoxO1 in DA neurons is an important transcriptional fact

159 However, the homoeostatic role of FoxO1 in DA system has not been investigated.

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

161 d mechanistic analysis of insulin control of FOXO1 in human adipocytes obtained from non-diabetic sub

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

163 sults also have implications for the role of FOXO1 in lymphomagenesis because they suggest that const

164 To better define the role of FoxO1 in mediating insulin effects in the liver, we gene

165 Endothelial-restricted deletion of FOXO1 in mice induces a profound increase in EC prolifer

166 sed beta-cell mass, islets from mice lacking Foxo1 in pancreatic or endocrine progenitors responded p

167 The function of FOXO1 in sustaining the DZ program involved the trans-ac

168 In contrast, ablation of Foxo1 in terminally differentiated beta-cells did not in

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

170 Furthermore, activation of Foxo1 in the liver is sufficient to suppress albumin exp

171 FOXO1 in these cells is also involved in regulation of e

172 of this pathway, we investigated the role of FOXO1 in toxicity of BCR pathway inhibition.

173 Forkhead transcriptional factor O1 (FoxO1) in the hypothalamus plays a crucial role in media

174 Concomitant deletion of Forkhead Box O1 (Foxo1) in these livers rescued the decreased albumin sec

175 Thus, Foxo1 inactivation is essential for the migration of aTr

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

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

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

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

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

181 AS1842856, a FoxO1 inhibitor, also suppressed TLR4 signaling.

182 We conclude that Foxo1 integrates cues that determine developmental timin

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

184 s that the reduction of the concentration of FOXO1 is a consequence of attenuation of mTORC1, which d

185 In this study, we show that, in T cells, Foxo1 is a negative regulator of the Th17 program.

186 mical SYK inhibitor R406, demonstrating that FOXO1 is also required for R406-induced cell death.

187 e forkhead box O (FOXO) transcription factor FOXO1 is an essential regulator of vascular growth that

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

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

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

191 milar to the myogenesis time point when PAX3-FOXO1 is expressed.

192 Here we report that FoxO1 is highly expressed in DA neurons and mice lacking

193 We show that FOXO1 is mainly phosphorylated through mTORC2-mediated p

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

195 These results demonstrate that FOXO1 is required for SYK and AKT inhibitor-induced toxi

196 Because forkhead box O1 (FOXO1) is a major effector of this pathway, we investiga

197 genes involved in T cell responses (BCL11B, FOXO1, KIF13B, PAWR, SOX4, SYK), actin cytoskeleton orga

198 epatic transcriptome profiling in mice after FOXO1 knockdown in the absence or presence of TH, and we

199 Finally, neutrophil-selective FOXO1 knockdown leads to defective placentation and comp

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

201 n by generating an allelic series of somatic Foxo1 knockouts at different stages of pancreatic develo

202 RP neuron-specific Gpr17 knockouts phenocopy FOXO1 knockouts in the same cell type, thus supporting o

203 Moreover, FoxO1 KO(DAT) mice exhibit an increased sucrose preferen

204 acking FoxO1 specifically in the DA neurons (FoxO1 KO(DAT)) show markedly increased energy expenditur

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

206 signaling decreased phospho-AKT and phospho-FOXO1 levels and triggered FOXO1-driven gene expression.

207 Furthermore, Phlpp1 deficiency diminished FoxO1 levels leading to increased expression of Fgf18, M

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

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

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

211 ability to bind chromatin and the effect of FoxO1 loss on recruitment of neighboring transcription f

212 d loci, including IBTK, RXRA-COL5A1, COL5A1, FOXO1, LRRK1 and ZNF469 (P < 1.25E-3).

213 wn about how insulin regulates FOXO1 and how FOXO1 may contribute to insulin resistance in adipocytes

214 gnaling to regulate forkhead box protein O1 (FOXO1) may be the most important mechanism for insulin t

215 omotes cytoplasmic translocation, inhibiting FoxO1-mediated transactivation.

216 FOXO1-mediated transcriptional repression of UBE3A was s

217 Expression of the Foxo1 mutant at a lower dose was sufficient to deplete t

218 ll-specific expression of an Akt-insensitive Foxo1 mutant prevented downregulation of lymphoid organ

219 Introduction of constitutively active FOXO1 mutant triggered cell cycle arrest and apoptosis,

220 heostat of vascular expansion and define the FOXO1-MYC transcriptional network as a novel metabolic c

221 ditional deletion in NK cells, we found that Foxo1 negatively controlled NK cell differentiation and

222 Foxo1 negatively regulated the pathogenicity of Th17 cel

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

224 ng MAPK signaling had virtually no effect on FoxO1 nuclear export in controls, in contrast to attenua

225 e Akt pathway, while ERK phosphorylation and FoxO1 nuclear export occur independently of insulin sign

226 d box protein O1 (FOXO1) phosphorylation and FOXO1 nuclear export.

227 ion and downstream Akt activation, increased FOXO1 nuclear localization and transcriptional activatio

228 Moreover, TH increased FOXO1 nuclear localization, DNA binding, and target gene

229 the winged helix DNA binding motif curtails FoxO1 nucleosome binding.

230 ndent phosphorylation of Akt on Ser(473) and FoxO1/O3a on Thr(24/32) in leukocytes and neutrophils.

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

232 We have previously demonstrated that FoxO1 opens and remodels chromatin assembled from the IG

233 of naive T cells with specific inhibitor of Foxo1 or inhibitors of the PI3K/Akt pathway acting upstr

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

235 Moreover, restoration of MYC signalling in FOXO1-overexpressing endothelium normalizes metabolic ac

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

237 PAX3-FOXO1 (paired box gene 3 fused with forkhead box O1) fus

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

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

240 le upstream regulatory kinases in the PAX3/7-FOXO1 pathway.

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

242 gene transcription by reducing AKT-dependent FOXO1 phosphorylation in a THRB1-dependent manner.

243 However, the impact of FoxO1 phosphorylation on its ability to bind chromatin a

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

245 and insulin signaling due to its effects on FOXO1 phosphorylation.

246 This, in turn, led to decreased AKT and FOXO1 phosphorylation.

247 ctivation, promoted Forkhead box protein O1 (FOXO1) phosphorylation and FOXO1 nuclear export.

248 Here we show that the transcription factor Foxo1, previously demonstrated to promote Treg cell supp

249 Foxo1 promoted NK cell homing to lymph nodes by upregula

250 Insulin-mediated phosphorylation of FoxO1 promotes cytoplasmic translocation, inhibiting Fox

251 he data support the notion that deacetylated FoxO1 protects beta-cell function by limiting mitochondr

252 hyperglycaemia through reduction of hepatic FOXO1 protein and gluconeogenic gene expression.

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

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

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

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

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

258 We found that FOXO1 protein was reduced in Nr4a3-deficient DCs through

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

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

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

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

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

264 Conversely, forced expression of FOXO1 restricts vascular expansion and leads to vessel t

265 the PAX3 promoter interacts ectopically with FOXO1 sequences.

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

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

268 hly expressed in DA neurons and mice lacking FoxO1 specifically in the DA neurons (FoxO1 KO(DAT)) sho

269 involving PTEN and forkhead box protein O1 (Foxo1), supporting autoantibody generation and triggerin

270 Mechanistically, FOXO1 suppresses signalling by MYC (also known as c-MYC)

271 hepatocytes to activate Akt, which inhibits Foxo1 suppressing hepatic glucose production (HGP) and a

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

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

274 rphyrin (SnPP) or siRNA downregulated Pax3/7-FoxO1 target genes and induced a myogenic program in RMS

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

276 tumour-infiltrating Treg cells downregulated Foxo1 target genes more substantially.

277 We identified a subset of TH-stimulated FOXO1 target genes that required co-regulation by FOXO1

278 y activity is essential for a subset of PAX3-FOXO1 target genes.

279 her, they bind to regulatory regions of PAX3-FOXO1 target genes.

280 tor 17 (GPR17) was recently reported to be a Foxo1 target in agouti-related peptide (AGRP) neurons.

281 rdinated and sensitive regulation of hepatic FOXO1-target gene expression.

282 Targeting of FOXO1 therefore provides a potential therapeutic strateg

283 that ICOS signaling transiently inactivates FOXO1 to initiate a Tfh cell contingency that is complet

284 t consequence of their inability to transfer FOXO1 to T cells.

285 ORC1 with rapamycin reduces the abundance of FOXO1 to the levels in T2D.

286 proteins, including forkhead box protein 1 (FOXO1), to T cells.

287 In this study we show that FOXO1 transcription factor expression was restricted to

288 ing H3K36me2 and H3K27me3 on the promoter of FOXO1 (transcription factor of gluconeogenic genes).

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

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

291 CHD4 interacts with PAX3-FOXO1 via short DNA fragments.

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

293 Repression of DIO2 by FOXO1 was confirmed using its specific inhibitor AS18428

294 TH activation of FOXO1 was directly linked to an increase in SIRT1-MTORC2

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

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

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

298 pecific deletion of the transcription factor FOXO1, which reduces dendritic cell (DC) function.

299 In SSCs, Myc/Mycn are regulated by Foxo1, whose deficiency impairs SSC self-renewal.

300 Depletion of FOXO1 with short hairpin RNA led to almost complete resi