ライフサイエンスコーパス: COUP-TFII

1 COUP-TFII (also known as Nr2f2), a member of the nuclear

2 COUP-TFII (NR2F2), chicken ovalbumin upstream promoter-t

3 COUP-TFII also suppresses the metabolic regulator PGC-1

4 COUP-TFII and GATA2 are physically associated and repres

5 COUP-TFII colocalized with renin in the juxtaglomerular

6 COUP-TFII declines during adipogenesis in reciprocal fas

7 COUP-TFII deficiency at a late developmental stage resul

8 COUP-TFII enhanced the pro-lymphangiogenic actions of VE

9 COUP-TFII expression in TAM-R cells also inhibited 4-OHT

10 COUP-TFII is expressed in lateral plate mesoderm of the

11 COUP-TFII is highly expressed in the mesenchymal compone

12 COUP-TFII is one of the four known genes residing within

13 COUP-TFII mutants are defective in remodeling the primit

14 COUP-TFII protein expression level is high in undifferen

15 COUP-TFII represses genes critical for mitochondrial ele

16 COUP-TFII represses the expression of a number of proadi

17 COUP-TFII, a member of orphan nuclear receptors, is expr

18 COUP-TFII, an orphan member of the steroid receptor supe

19 COUP-TFII, an orphan nuclear receptor, is preferentially

20 COUP-TFII-overexpressing mice exhibited regenerative fai

21 at in the context of the MTP promoter, ARP-1/COUP-TFII (repressor) and a complex containing RXRalpha

22 These combined findings indicate that ARP-1/COUP-TFII acts as both a transcriptional repressor (of M

23 s from L35 cells contained 2-fold more ARP-1/COUP-TFII and 50% less RXRalpha than those from FAO cell

24 Co-transfection of an ARP-1/COUP-TFII expression vector showed that it enhances CYP7

25 ologic studies show that in L35 cells, ARP-1/COUP-TFII is bound to the DR1 element, whereas in FAO ce

26 This dual function of ARP-1/COUP-TFII may play an important role in determining the

27 Co-transfection studies show that ARP-1/COUP-TFII repressed MTP promoter activity by approximate

28 ream promoter transcription factor II (ARP-1/COUP-TFII) and retinoid X receptor (RXRalpha) as the pro

29 in upstream promoter transcription factor 2 (COUP-TFII) at the transcriptional and the post-transcrip

30 ed a conditional-knockout approach to ablate COUP-TFII specifically in the limbs.

31 In addition, COUP-TFII inactivation in a mammary gland mouse tumor mo

32 In addition, COUP-TFII is also expressed in the somites and skeletal

33 Also, COUP-TFII is required for appropriate development of the

34 Although COUP-TFII is likely to play a role in the development of

35 with overlapping binding sites for SF-1 and COUP-TFII in their promoter regions, but does not affect

36 SF-1, Sox14, Satb2, Fezf1, Dax1, Nkx2-2, and COUP-TFII, but interestingly, the highest expressed VMH

37 ereas Notch is expressed in the arteries and COUP-TFII in the veins, the lymphatics express all 3 cel

38 ctrophoretic mobility shift experiments, and COUP-TFII/ARP-1-containing complexes were detected in He

39 cooperate during post-natal myogenesis, and COUP-TFII is critical for the accelerated skeletal muscl

40 Here, we show that COUP-TFI (Nr2f1) and COUP-TFII (Nr2f2) are highly expressed in the progenitor

41 unctional link between hedgehog proteins and COUP-TFII, factors that are vital for epithelial-mesench

42 On the contrary, Prox1 and COUP-TFII attenuate vascular endothelial growth factor s

43 d that Notch signal down-regulates Prox1 and COUP-TFII through Hey1 and Hey2 and that activated Notch

44 endothelial genes such as SOX18, SMAD6, and COUP-TFII was regulated by ensuring efficient RNA polyme

45 ted the hypothesis that reduced COUP-TFI and COUP-TFII correlate with TAM resistance.

46 Phenotype analysis of COUP-TFI and COUP-TFII single-gene conditional knockout mouse models

47 as the orphan nuclear receptors COUP-TFI and COUP-TFII.

48 luding cell proliferation and migration, are COUP-TFII-dependent and cell-autonomous processes.

49 erial markers whereas venous markers such as COUP-TFII are normally expressed, suggesting that mutant

50 2 transcription activator hub and the BCL11A/COUP-TFII/GATA-1 transcription repressor hub.

51 Because COUP-TFII has little impact on normal adult physiologica

52 The functional counteraction between COUP-TFII and SMAD4 is reinforced by genetically enginee

53 ruction of the TGF-beta-dependent barrier by COUP-TFII is crucial for the progression of PTEN-mutant

54 iminishes the inhibitory effects elicited by COUP-TFII ablation.

55 T cells and tumor inhibition are mediated by COUP-TFII-induced vascular adhesion receptors.

56 ts in female embryos is actively promoted by COUP-TFII, which suppresses a mesenchyme-epithelium cros

57 ndings suggest that lifting of repression by COUP-TFII may be an important mechanism that promotes in

58 increased when transcriptional repression by COUP-TFII was blocked.

59 in cytokine-treated Ad12-transformed cells, COUP-TFII is able to repress activation of class I trans

60 In conclusion, COUP-TFII and THRA cooperate during post-natal myogenesi

61 UP-TFII in the CNS, we generated conditional COUP-TFII knockout mice using a tissue-specific NSE-Cre

62 region on 15q26 to an interval that contains COUP-TFII and only eight other known genes.

63 phosphatase 2A activity, and that decreased COUP-TFII expression resulted in gamma-globin reactivati

64 endothelial cells resulted in downregulated COUP-TFII expression and aberrant expression of arterial

65 mice, suggesting a causal effect of elevated COUP-TFII levels on development of dilated cardiomyopath

66 ty during myogenesis and found that elevated COUP-TFII activity resulted in inefficient skeletal musc

67 During mouse embryogenesis, COUP-TFII protein is highly detected in the mesenchymal

68 The endometrial COUP-TFII might modulate the signaling between the uteru

69 Pan-endothelial COUP-TFII overexpression induces ectopic addressin expre

70 nuclear receptors including ER, ESRRB, ERRy, COUP-TFII (NR2F2), RARa, EAR2 as well as traditional pio

71 Here, we examined COUP-TFII as a potential repressor of gamma-globin gene

72 nerated a mouse model ectopically expressing COUP-TFII in myogenic precursors to maintain COUP-TFII a

73 decrease in the percentage of LC expressing COUP-TFII.

74 The transcription factor COUP-TFII currently functions at the top of a signaling

75 ulation of downstream transcriptional factor COUP-TFII, which is involved in the regulation of gamma-

76 screening method to identify another factor, COUP-TFII/ARP-1, which also binds to the ATPA cis-acting

77 ite through which the transcription factors, COUP-TFII/ARP-1 and USF2, bind and exert their antagonis

78 In transiently transfected fibroblasts COUP-TFII acts at gAF1/PCK1 to inhibit PPARgamma/RXR act

79 tients with 15q26 deletions, we did not find COUP-TFII mutations in 73 CDH samples.

80 Conditional ablation of floxed COUP-TFII by Nkx3-2Cre recombinase in the gastric mesenc

81 analysis has revealed an obligatory role for COUP-TFII in limb bud outgrowth since mutant cells are u

82 analysis indicated that the binding site for COUP-TFII/ARP-1 in the ATPA regulatory element 1 is an i

83 We found COUP-TFII is expressed in the mesenchyme and the epithel

84 We generated COUP-TFII mouse mutants, using Rx-Cre (RxCre;COUP-TFII(F

85 non-coding transcript Bgl3, and we identify COUP-TFII binding sites within the Bgl3 locus.

86 n upstream promoter-transcription factor II (COUP-TFII) has been shown to inhibit myogenesis and skel

87 n upstream promoter-transcription factor II (COUP-TFII) hyperactivity as a contributing factor underl

88 n upstream promoter transcription factor II (COUP-TFII) in a dose-dependent manner.

89 n Upstream Promoter-Transcription Factor II (COUP-TFII) in Leydig cell (LC) steroidogenesis that may

90 n upstream promoter transcription factor II (COUP-TFII) in the regulation of renin gene expression.

91 n Upstream Promoter-Transcription Factor II (COUP-TFII) is an important coordinator of glucose homeos

92 n upstream promoter transcription factor II (COUP-TFII) is the predominant nuclear receptor bound to

93 n upstream promoter-transcription factor II (COUP-TFII) promoter that binds to a factor distinct from

94 ovalbumin upstream-transcription factor II (COUP-TFII) that promote or inhibit divergent pathways of

95 ovalbumin upstream transcription factor II (COUP-TFII) was decreased 40% at 16 hours.

96 n upstream promoter-transcription factor II (COUP-TFII), a member of the nuclear receptor family, is

97 n upstream promoter-transcription factor II (COUP-TFII), a member of the nuclear receptor superfamily

98 n upstream promoter-transcription factor II (COUP-TFII).

99 n upstream promoter transcription factor II (COUP-TFII).

100 n upstream promoter transcription factor II (COUP-TFII, also known as Nr2f2) is required for the spec

101 e we show that COUP transcription factor II (COUP-TFII, also known as NR2F2), a member of the nuclear

102 icken ovalbumin upstream promoter-factor II (COUP-TFII, or Nr2f2) persists during myogenic differenti

103 n upstream promoter-transcription factor II (COUP-TFII; Nr2f2) is expressed in adipose tissue in vivo

104 Taken together, our results implicate COUP-TFII as a critical factor in tumor angiogenesis thr

105 t not a mutant promoter that is defective in COUP-TFII/ARP-1-binding.

106 ll culture studies, mutant mice deficient in COUP-TFII have lower renin expression than their control

107 nd vascular remodeling, is down-regulated in COUP-TFII mutants.

108 cre/loxP system to conditionally inactivate COUP-TFII in the ovary and uterus.

109 Further, E(2) increased COUP-TFII transcription in MCF-7, but not TAM-R, cells.

110 4-OHT increased COUP-TFII-ERalpha interaction approximately 2-fold in MC

111 identify the vicious cycle of inflammation, COUP-TFII, VEGF-C, and lymphangiogenesis in the endometr

112 Last, COUP-TFII haploinsufficiency attenuates the progression

113 e DBP neither causes persistence of fetal LC COUP-TFII nor reduces ITT, whereas DES-exposure of mice

114 tly prevented the age-related decrease in LC COUP-TFII expression and the normal increases in LC size

115 COUP-TFII in myogenic precursors to maintain COUP-TFII activity during myogenesis and found that elev

116 ITT, whereas DES-exposure of mice maintains COUP-TFII expression in fetal LC and decreases ITT, as i

117 Most importantly, this miRNA-COUP-TFII-FOXM1-CENPF regulatory axis is also involved i

118 Moreover, COUP-TFII silencing reverses the transcriptomic profile

119 Here, we report that in murine myoblasts COUP-TFII interacts with THRA and modulates THRA binding

120 ggesting that a major function of myocardial COUP-TFII is to determine atrial identity.

121 Here, we show that myocardial COUP-TFII overexpression causes heart failure in mice, s

122 Our results define an NKX-COUP-TFII morphogenetic code that targets expression of

123 We identify conserved NKX-COUP-TFII composite elements (NCCE) in regulatory region

124 ied by the master regulators, namely, Notch, COUP-TFII, and Prox1.

125 the transcriptional factors OCT4 and NR2F2 (COUP-TFII) and the miRNA miR-302 are linked in a regulat

126 cification, while the orphan receptor nr2f2 (COUP-TFII) has been implicated in venous specification.

127 e role of the orphan nuclear receptor NR2F2 (COUP-TFII) in FLC development.

128 We show that nuclear COUP-TFII expression in fetal rat LC relates inversely t

129 Conditional ablation of COUP-TFII at an early embryonic stage resulted in failed

130 Conditional ablation of COUP-TFII in adults severely compromised neoangiogenesis

131 Ablation of COUP-TFII in endothelial cells enables veins to acquire

132 Ablation of COUP-TFII in mice led to higher bone density, increased

133 Ablation of COUP-TFII in the brain resulted in malformation of the l

134 Ablation of COUP-TFII in the foregut mesenchyme, including the posth

135 Conditional ablation of COUP-TFII in the tumor microenvironment severely comprom

136 mammary-gland tumor model in the absence of COUP-TFII.

137 et factor that is required for activation of COUP-TFII-, Islet1-, and Gli response element-dependent

138 However, the deficiency of COUP-TFII did not further diminish the renin expression

139 Deletion of COUP-TFII at E7.5 results in improper differentiation of

140 ortant question of whether downregulation of COUP-TFII expression is required for proper muscle cell

141 siRNA-mediated downregulation of COUP-TFII in cultured primary human LECs demonstrated th

142 amine treatment, we showed downregulation of COUP-TFII level in the stomach, suggesting COUP-TFII as

143 Furthermore, ectopic expression of COUP-TFII in endothelial cells results in the fusion of

144 show an age-related decline in expression of COUP-TFII in human fetal LC, this mechanism may also be

145 Ectopic expression of COUP-TFII in murine SCs led to Duchenne-like dystrophy i

146 e X-gal staining to follow the expression of COUP-TFII in the developing stomach.

147 Consistently, over-expression of COUP-TFII led to the completely opposite effects.

148 w that ectopic pan-endothelial expression of COUP-TFII, a master transcription factor for venous deve

149 The embryonic expression of COUP-TFII, an orphan nuclear receptor, suggests that it

150 lso maintain/induce LC nuclear expression of COUP-TFII.

151 To analyze the physiological function of COUP-TFII during organogenesis, we used the cre/loxP sys

152 To address the function of COUP-TFII in the CNS, we generated conditional COUP-TFII

153 1 positively correlates with the increase of COUP-TFII-FOXM1-CENPF activity in clinical PCa data sets

154 n interesting possibility that inhibition of COUP-TFII may offer a therapeutic approach for anticance

155 Furthermore, inhibition of COUP-TFII preserved SC function and counteracted the mus

156 Conversely, knockdown of COUP-TFII in TAM-S MCF-7 cells blocked growth inhibitory

157 Accordingly, knockdown of COUP-TFII in the clonal renin-producing cell lines As4.1

158 Knockdown of COUP-TFII or cAMP-binding protein (CREB), which is the a

159 Because of the early embryonic lethality of COUP-TFII knockout mice, the role of COUP-TFII during li

160 phenotypic modulation by different levels of COUP-TFII in arterial and venous ECs, and suggest COUP-T

161 Loss of COUP-TFII in the limbs leads to hypoplastic skeletal mus

162 we show that tissue-specific null mutants of COUP-TFII exhibit Bochdalek-type CDH, the most common fo

163 A null mutation of COUP-TFII results in the malformation of the heart and b

164 Overexpression of COUP-TFII in the mouse prostate epithelium cooperates wi

165 Overexpression of COUP-TFII prevents adipogenesis, whereas shRNA-mediated

166 Furthermore, reduction of COUP-TFII allows uncommitted fibroblasts to be different

167 genesis, whereas shRNA-mediated reduction of COUP-TFII promotes differentiation, as shown by increase

168 Importantly, reexpression of COUP-TFII in TAM-S cells to levels comparable to those i

169 Furthermore, down-regulation of COUP-TFII expression with small interfering RNA (siRNA)

170 ghlight the importance of down-regulation of COUP-TFII signaling to allow for the induction of factor

171 lity of COUP-TFII knockout mice, the role of COUP-TFII during limb development has not been determine

172 ore, in order to study the potential role of COUP-TFII in limb and skeletal muscle development, we by

173 tudy describes an important maternal role of COUP-TFII in regulating the placentation.

174 er, our findings reveal a regulatory role of COUP-TFII in the development of muscular dystrophy and o

175 To understand the functional significance of COUP-TFII expression in the steroidogenic factor 1 neuro

176 The biological significance of COUP-TFII in prostate carcinogenesis is substantiated by

177 Silencing of COUP-TFII expression restores in vitro myogenic potentia

178 Specifically, we found that suppression of COUP-TFII in venous ECs switched its phenotype toward pr

179 roinflammatory cytokines, via suppression of COUP-TFII level, induce VEGF-C overexpression.

180 rp1 and Nrp2 genes are the direct targets of COUP-TFII in the telencephalon in vivo.

181 We also show that once COUP-TFII expression in LC has switched off, it is re-in

182 These findings indicate that the persistent COUP-TFII expression in THRA-PV mice is responsible for

183 al role in induction of arterial phenotypes, COUP-TFII is required to maintain the venous EC identity

184 among many other cardiac genes, as potential COUP-TFII direct targets.

185 BRG1 promotes COUP-TFII expression by binding conserved regulatory ele

186 he chromatin-remodeling enzyme BRG1 promotes COUP-TFII expression in venous endothelial cells during

187 the first description of a factor promoting COUP-TFII expression in vascular endothelium and highlig

188 However, the orphan nuclear receptor COUP-TFII as well as the Notch signaling pathway, which

189 origenesis to show that the nuclear receptor COUP-TFII is essential to regulate the balance between p

190 3 cooperatively with venous nuclear receptor COUP-TFII to activate transcription.

191 The nuclear orphan receptor COUP-TFII is widely expressed in multiple tissues and or

192 Binding of the orphan nuclear receptor, COUP-TFII/ARP-1, to the ATPA regulatory element 1 was co

193 Recombinant COUP-TFII expressed in HepG2 or COS-1 cells were found t

194 These data indicate that reduced COUP-TFII expression correlates with acquired TAM resist

195 s, yet nothing is known about what regulates COUP-TFII expression in veins.

196 we report that the venous EC fate regulator COUP-TFII is expressed in LECs throughout development an

197 OUP-TFII binds to an imperfect direct repeat COUP-TFII recognition sequence (termed hereafter proxDR)

198 ay, which regulates the downstream repressor COUP-TFII by inhibiting serine/threonine phosphatase 2A

199 hroid repressor GATA-1 and general repressor COUP-TFII to form respectively the NF-Y/GATA-2 transcrip

200 ich there is strong binding of the repressor COUP-TFII and lack of binding of the activator NF-kappaB

201 COUP-TFII mouse mutants, using Rx-Cre (RxCre;COUP-TFII(F/F)), to study its function in telencephalon

202 Cardiomyocyte-specific COUP-TFII ablation produces ventricularized atria that e

203 d hypothalamic ventromedial nucleus-specific COUP-TFII KO mice using the cyclization recombination/lo

204 TFII in arterial and venous ECs, and suggest COUP-TFII may play an important role in the different su

205 lation of VEGF/VEGFR-2 signaling, suggesting COUP-TFII as a candidate target for antiangiogenic thera

206 f COUP-TFII level in the stomach, suggesting COUP-TFII as a target of hedgehog signaling in the stoma

207 nto a life-threatening disease, and supports COUP-TFII as a potential drug target for the interventio

208 the murine model, suggesting that targeting COUP-TFII is a potential treatment for DMD.

209 e in human breast cancer cell lines and that COUP-TFII plays a role in regulating the growth inhibito

210 We conclude that COUP-TFII stimulates the transcriptional activity of the

211 We further demonstrate that COUP-TFII directs the plasticity of mesenchymal precurso

212 Taken together, our results demonstrate that COUP-TFII plays an early role in limb bud outgrowth but

213 Taken together, our data demonstrate that COUP-TFII represents an endogenous suppressor of adipoge

214 We further demonstrated that COUP-TFII also reduces the activation of focal adhesion

215 rotein-DNA binding studies demonstrated that COUP-TFII binds to an imperfect direct repeat COUP-TFII

216 Recently we have demonstrated that COUP-TFII expression in the hypothalamus is restricted t

217 Using ChIP assays, we demonstrated that COUP-TFII was recruited to the promoter region of IGF-1

218 ore, cotransfection assays demonstrated that COUP-TFII/ARP-1 inhibits the USF2-mediated activation of

219 Mechanistically, we determined that COUP-TFII coordinated a regenerative program through com

220 In this study, we discovered that COUP-TFII, a transcription factor critical for establish

221 We found that COUP-TFII expression is suppressed by SCF through phosph

222 We found that COUP-TFII functions as a coregulator of Prox1 to control

223 We found that COUP-TFII plays a cell-autonomous role in endothelial ce

224 Thus, our results indicate that COUP-TFII regulates growth and maturation of the mouse p

225 urin transgenic mouse model, indicating that COUP-TFII may serve as a therapeutic target for the trea

226 ficient mice, which supports the notion that COUP-TFII controls Angiopoietin-1/Tie2 signaling to regu

227 Collectively, our results reveal that COUP-TFII confers atrial identity through direct binding

228 Mechanistic investigations revealed that COUP-TFII suppressed vascular endothelial growth factor

229 Mobility shift assays revealed that COUP-TFII/ARP-1 and USF2 compete for binding to the ATPA

230 Here, we show that COUP-TFII (also known as Nr2f2), a member of the orphan

231 Here, we show that COUP-TFII (also known as Nr2f2), an orphan member of the

232 We show that COUP-TFII acts downstream of hedgehog signaling and is r

233 Importantly, we show that COUP-TFII directly regulates the expression of both Eya1

234 Further studies show that COUP-TFII is a critical factor controlling metastatic ge

235 Altogether our data show that COUP-TFII is involved in the control of renin gene expre

236 We showed that COUP-TFII directly regulates the transcription of Angiop

237 ure and in vivo mouse models, we showed that COUP-TFII hinders myogenic development by repressing myo

238 Functional assays in HeLa cells showed that COUP-TFII/ARP-1 represses the ATPA promoter activity in

239 These data suggest that COUP-TFII affects mitochondrial function, impairs metabo

240 the renin gene expression, we suggested that COUP-TFII may modulate this cAMP effect.

241 of tumor lymphangiogenesis, suggesting that COUP-TFII also regulates neo-lymphangiogenesis in the ad

242 ghout embryonic development, suggesting that COUP-TFII is involved in multiple aspects of embryogenes

243 Our finding suggests that COUP-TFII is a likely contributor to the formation of CD

244 This down-regulation suggests that COUP-TFII may be required for bidirectional signaling be

245 We report for the first time that COUP-TFII, but not COUP-TFI, is reduced in three antiest

246 ur findings reveal, for the first time, that COUP-TFII plays a central role in the specification of m

247 However, although the COUP-TFII nuclear receptor has recently been shown to re

248 ores the angiogenic defects exhibited by the COUP-TFII-deficient mice, which supports the notion that

249 generation of a lacZ knock-in allele in the COUP-TFII locus in mice allows us to use X-gal staining

250 In the COUP-TFII mutant heart, the atria and sinus venosus fail

251 Targeted deletion of the COUP-TFII gene results in embryonic lethality with defec

252 ypassed the early embryonic lethality of the COUP-TFII mutant by using two methods.

253 pecific miRNAs through the regulation of the COUP-TFII-FOXM1-CENPF cascade in PCa metastasis and drug

254 Overexpression of USF2 reversed the COUP-TFII/ARP-1-mediated repression of the ATPA promoter

255 ing conserved regulatory elements within the COUP-TFII promoter and remodeling chromatin to make the

256 Therefore, COUP-TFII expression levels in the ventromedial nucleus

257 XM1 and CENPF by these miRNAs occurs through COUP-TFII, a member of the orphan nuclear receptors fami

258 Thus, COUP-TFII has a critical role in repressing Notch signal

259 Thus, COUP-TFII is a critical factor that controls lymphangiog

260 ntiated by patient sample analysis, in which COUP-TFII expression or activity is tightly correlated w

261 /PCK1 is a pleiotropic element through which COUP-TFII inhibits premature PEPCK expression, and perha

262 by supershifting the corresponding band with COUP-TFII-specific antibodies.

263 ECs with COUP-TFII knockdown also readily undergo endothelial-to-

264 ness and lipid metabolism and interacts with COUP-TFII to form a transcriptional complex.

265 Finally, YAP1, COUP-TFII, and miR-21 are detected in the extracellular