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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 ed a conditional-knockout approach to ablate COUP-TFII specifically in the limbs.
30                                 In addition, COUP-TFII inactivation in a mammary gland mouse tumor mo
31                                 In addition, COUP-TFII is also expressed in the somites and skeletal
32                                        Also, COUP-TFII is required for appropriate development of the
33                                     Although COUP-TFII is likely to play a role in the development of
34  with overlapping binding sites for SF-1 and COUP-TFII in their promoter regions, but does not affect
35 SF-1, Sox14, Satb2, Fezf1, Dax1, Nkx2-2, and COUP-TFII, but interestingly, the highest expressed VMH
36 ereas Notch is expressed in the arteries and COUP-TFII in the veins, the lymphatics express all 3 cel
37 ctrophoretic mobility shift experiments, and COUP-TFII/ARP-1-containing complexes were detected in He
38      Here, we show that COUP-TFI (Nr2f1) and COUP-TFII (Nr2f2) are highly expressed in the progenitor
39 unctional link between hedgehog proteins and COUP-TFII, factors that are vital for epithelial-mesench
40                   On the contrary, Prox1 and COUP-TFII attenuate vascular endothelial growth factor s
41 d that Notch signal down-regulates Prox1 and COUP-TFII through Hey1 and Hey2 and that activated Notch
42  endothelial genes such as SOX18, SMAD6, and COUP-TFII was regulated by ensuring efficient RNA polyme
43 ted the hypothesis that reduced COUP-TFI and COUP-TFII correlate with TAM resistance.
44           Phenotype analysis of COUP-TFI and COUP-TFII single-gene conditional knockout mouse models
45 as the orphan nuclear receptors COUP-TFI and COUP-TFII.
46 luding cell proliferation and migration, are COUP-TFII-dependent and cell-autonomous processes.
47 erial markers whereas venous markers such as COUP-TFII are normally expressed, suggesting that mutant
48 2 transcription activator hub and the BCL11A/COUP-TFII/GATA-1 transcription repressor hub.
49                                      Because COUP-TFII has little impact on normal adult physiologica
50         The functional counteraction between COUP-TFII and SMAD4 is reinforced by genetically enginee
51 ruction of the TGF-beta-dependent barrier by COUP-TFII is crucial for the progression of PTEN-mutant
52 iminishes the inhibitory effects elicited by COUP-TFII ablation.
53 ts in female embryos is actively promoted by COUP-TFII, which suppresses a mesenchyme-epithelium cros
54 ndings suggest that lifting of repression by COUP-TFII may be an important mechanism that promotes in
55 increased when transcriptional repression by COUP-TFII was blocked.
56  in cytokine-treated Ad12-transformed cells, COUP-TFII is able to repress activation of class I trans
57 UP-TFII in the CNS, we generated conditional COUP-TFII knockout mice using a tissue-specific NSE-Cre
58 region on 15q26 to an interval that contains COUP-TFII and only eight other known genes.
59  phosphatase 2A activity, and that decreased COUP-TFII expression resulted in gamma-globin reactivati
60  endothelial cells resulted in downregulated COUP-TFII expression and aberrant expression of arterial
61 mice, suggesting a causal effect of elevated COUP-TFII levels on development of dilated cardiomyopath
62 ty during myogenesis and found that elevated COUP-TFII activity resulted in inefficient skeletal musc
63                  During mouse embryogenesis, COUP-TFII protein is highly detected in the mesenchymal
64                              The endometrial COUP-TFII might modulate the signaling between the uteru
65                            Here, we examined COUP-TFII as a potential repressor of gamma-globin gene
66 nerated a mouse model ectopically expressing COUP-TFII in myogenic precursors to maintain COUP-TFII a
67  decrease in the percentage of LC expressing COUP-TFII.
68                     The transcription factor COUP-TFII currently functions at the top of a signaling
69 ulation of downstream transcriptional factor COUP-TFII, which is involved in the regulation of gamma-
70 screening method to identify another factor, COUP-TFII/ARP-1, which also binds to the ATPA cis-acting
71 ite through which the transcription factors, COUP-TFII/ARP-1 and USF2, bind and exert their antagonis
72       In transiently transfected fibroblasts COUP-TFII acts at gAF1/PCK1 to inhibit PPARgamma/RXR act
73 tients with 15q26 deletions, we did not find COUP-TFII mutations in 73 CDH samples.
74               Conditional ablation of floxed COUP-TFII by Nkx3-2Cre recombinase in the gastric mesenc
75 analysis has revealed an obligatory role for COUP-TFII in limb bud outgrowth since mutant cells are u
76 analysis indicated that the binding site for COUP-TFII/ARP-1 in the ATPA regulatory element 1 is an i
77                                     We found COUP-TFII is expressed in the mesenchyme and the epithel
78                                 We generated COUP-TFII mouse mutants, using Rx-Cre (RxCre;COUP-TFII(F
79  non-coding transcript Bgl3, and we identify COUP-TFII binding sites within the Bgl3 locus.
80 n upstream promoter-transcription factor II (COUP-TFII) has been shown to inhibit myogenesis and skel
81 n upstream promoter-transcription factor II (COUP-TFII) hyperactivity as a contributing factor underl
82 n upstream promoter transcription factor II (COUP-TFII) in a dose-dependent manner.
83 n Upstream Promoter-Transcription Factor II (COUP-TFII) in Leydig cell (LC) steroidogenesis that may
84 n upstream promoter transcription factor II (COUP-TFII) in the regulation of renin gene expression.
85 n Upstream Promoter-Transcription Factor II (COUP-TFII) is an important coordinator of glucose homeos
86 n upstream promoter transcription factor II (COUP-TFII) is the predominant nuclear receptor bound to
87 n upstream promoter-transcription factor II (COUP-TFII) promoter that binds to a factor distinct from
88  ovalbumin upstream-transcription factor II (COUP-TFII) that promote or inhibit divergent pathways of
89  ovalbumin upstream transcription factor II (COUP-TFII) was decreased 40% at 16 hours.
90 n upstream promoter-transcription factor II (COUP-TFII), a member of the nuclear receptor family, is
91 n upstream promoter-transcription factor II (COUP-TFII), a member of the nuclear receptor superfamily
92 n upstream promoter transcription factor II (COUP-TFII).
93 n upstream promoter transcription factor II (COUP-TFII, also known as Nr2f2) is required for the spec
94 e we show that COUP transcription factor II (COUP-TFII, also known as NR2F2), a member of the nuclear
95 n upstream promoter-transcription factor II (COUP-TFII; Nr2f2) is expressed in adipose tissue in vivo
96        Taken together, our results implicate COUP-TFII as a critical factor in tumor angiogenesis thr
97 t not a mutant promoter that is defective in COUP-TFII/ARP-1-binding.
98 ll culture studies, mutant mice deficient in COUP-TFII have lower renin expression than their control
99 nd vascular remodeling, is down-regulated in COUP-TFII mutants.
100  cre/loxP system to conditionally inactivate COUP-TFII in the ovary and uterus.
101                      Further, E(2) increased COUP-TFII transcription in MCF-7, but not TAM-R, cells.
102                              4-OHT increased COUP-TFII-ERalpha interaction approximately 2-fold in MC
103                                        Last, COUP-TFII haploinsufficiency attenuates the progression
104 e DBP neither causes persistence of fetal LC COUP-TFII nor reduces ITT, whereas DES-exposure of mice
105 tly prevented the age-related decrease in LC COUP-TFII expression and the normal increases in LC size
106 COUP-TFII in myogenic precursors to maintain COUP-TFII activity during myogenesis and found that elev
107  ITT, whereas DES-exposure of mice maintains COUP-TFII expression in fetal LC and decreases ITT, as i
108                 Most importantly, this miRNA-COUP-TFII-FOXM1-CENPF regulatory axis is also involved i
109 ggesting that a major function of myocardial COUP-TFII is to determine atrial identity.
110                Here, we show that myocardial COUP-TFII overexpression causes heart failure in mice, s
111 ied by the master regulators, namely, Notch, COUP-TFII, and Prox1.
112  the transcriptional factors OCT4 and NR2F2 (COUP-TFII) and the miRNA miR-302 are linked in a regulat
113 cification, while the orphan receptor nr2f2 (COUP-TFII) has been implicated in venous specification.
114                         We show that nuclear COUP-TFII expression in fetal rat LC relates inversely t
115                      Conditional ablation of COUP-TFII at an early embryonic stage resulted in failed
116                      Conditional ablation of COUP-TFII in adults severely compromised neoangiogenesis
117                                  Ablation of COUP-TFII in endothelial cells enables veins to acquire
118                                  Ablation of COUP-TFII in mice led to higher bone density, increased
119                                  Ablation of COUP-TFII in the brain resulted in malformation of the l
120                                  Ablation of COUP-TFII in the foregut mesenchyme, including the posth
121                      Conditional ablation of COUP-TFII in the tumor microenvironment severely comprom
122  mammary-gland tumor model in the absence of COUP-TFII.
123 et factor that is required for activation of COUP-TFII-, Islet1-, and Gli response element-dependent
124                   However, the deficiency of COUP-TFII did not further diminish the renin expression
125                                  Deletion of COUP-TFII at E7.5 results in improper differentiation of
126 ortant question of whether downregulation of COUP-TFII expression is required for proper muscle cell
127             siRNA-mediated downregulation of COUP-TFII in cultured primary human LECs demonstrated th
128 amine treatment, we showed downregulation of COUP-TFII level in the stomach, suggesting COUP-TFII as
129           Furthermore, ectopic expression of COUP-TFII in endothelial cells results in the fusion of
130 show an age-related decline in expression of COUP-TFII in human fetal LC, this mechanism may also be
131                        Ectopic expression of COUP-TFII in murine SCs led to Duchenne-like dystrophy i
132 e X-gal staining to follow the expression of COUP-TFII in the developing stomach.
133             Consistently, over-expression of COUP-TFII led to the completely opposite effects.
134                  The embryonic expression of COUP-TFII, an orphan nuclear receptor, suggests that it
135 lso maintain/induce LC nuclear expression of COUP-TFII.
136     To analyze the physiological function of COUP-TFII during organogenesis, we used the cre/loxP sys
137                   To address the function of COUP-TFII in the CNS, we generated conditional COUP-TFII
138 1 positively correlates with the increase of COUP-TFII-FOXM1-CENPF activity in clinical PCa data sets
139 n interesting possibility that inhibition of COUP-TFII may offer a therapeutic approach for anticance
140                   Furthermore, inhibition of COUP-TFII preserved SC function and counteracted the mus
141                     Conversely, knockdown of COUP-TFII in TAM-S MCF-7 cells blocked growth inhibitory
142                    Accordingly, knockdown of COUP-TFII in the clonal renin-producing cell lines As4.1
143                                 Knockdown of COUP-TFII or cAMP-binding protein (CREB), which is the a
144  Because of the early embryonic lethality of COUP-TFII knockout mice, the role of COUP-TFII during li
145 phenotypic modulation by different levels of COUP-TFII in arterial and venous ECs, and suggest COUP-T
146                                      Loss of COUP-TFII in the limbs leads to hypoplastic skeletal mus
147 we show that tissue-specific null mutants of COUP-TFII exhibit Bochdalek-type CDH, the most common fo
148                           A null mutation of COUP-TFII results in the malformation of the heart and b
149                            Overexpression of COUP-TFII in the mouse prostate epithelium cooperates wi
150                            Overexpression of COUP-TFII prevents adipogenesis, whereas shRNA-mediated
151                    Furthermore, reduction of COUP-TFII allows uncommitted fibroblasts to be different
152 genesis, whereas shRNA-mediated reduction of COUP-TFII promotes differentiation, as shown by increase
153                 Importantly, reexpression of COUP-TFII in TAM-S cells to levels comparable to those i
154              Furthermore, down-regulation of COUP-TFII expression with small interfering RNA (siRNA)
155 ghlight the importance of down-regulation of COUP-TFII signaling to allow for the induction of factor
156 lity of COUP-TFII knockout mice, the role of COUP-TFII during limb development has not been determine
157 ore, in order to study the potential role of COUP-TFII in limb and skeletal muscle development, we by
158 tudy describes an important maternal role of COUP-TFII in regulating the placentation.
159 er, our findings reveal a regulatory role of COUP-TFII in the development of muscular dystrophy and o
160 To understand the functional significance of COUP-TFII expression in the steroidogenic factor 1 neuro
161               The biological significance of COUP-TFII in prostate carcinogenesis is substantiated by
162   Specifically, we found that suppression of COUP-TFII in venous ECs switched its phenotype toward pr
163 rp1 and Nrp2 genes are the direct targets of COUP-TFII in the telencephalon in vivo.
164                       We also show that once COUP-TFII expression in LC has switched off, it is re-in
165 al role in induction of arterial phenotypes, COUP-TFII is required to maintain the venous EC identity
166 among many other cardiac genes, as potential COUP-TFII direct targets.
167                                BRG1 promotes COUP-TFII expression by binding conserved regulatory ele
168 he chromatin-remodeling enzyme BRG1 promotes COUP-TFII expression in venous endothelial cells during
169  the first description of a factor promoting COUP-TFII expression in vascular endothelium and highlig
170         However, the orphan nuclear receptor COUP-TFII as well as the Notch signaling pathway, which
171 origenesis to show that the nuclear receptor COUP-TFII is essential to regulate the balance between p
172                  The nuclear orphan receptor COUP-TFII is widely expressed in multiple tissues and or
173      Binding of the orphan nuclear receptor, COUP-TFII/ARP-1, to the ATPA regulatory element 1 was co
174                                  Recombinant COUP-TFII expressed in HepG2 or COS-1 cells were found t
175             These data indicate that reduced COUP-TFII expression correlates with acquired TAM resist
176 s, yet nothing is known about what regulates COUP-TFII expression in veins.
177  we report that the venous EC fate regulator COUP-TFII is expressed in LECs throughout development an
178 OUP-TFII binds to an imperfect direct repeat COUP-TFII recognition sequence (termed hereafter proxDR)
179 ay, which regulates the downstream repressor COUP-TFII by inhibiting serine/threonine phosphatase 2A
180 hroid repressor GATA-1 and general repressor COUP-TFII to form respectively the NF-Y/GATA-2 transcrip
181 ich there is strong binding of the repressor COUP-TFII and lack of binding of the activator NF-kappaB
182 COUP-TFII mouse mutants, using Rx-Cre (RxCre;COUP-TFII(F/F)), to study its function in telencephalon
183                       Cardiomyocyte-specific COUP-TFII ablation produces ventricularized atria that e
184 d hypothalamic ventromedial nucleus-specific COUP-TFII KO mice using the cyclization recombination/lo
185 TFII in arterial and venous ECs, and suggest COUP-TFII may play an important role in the different su
186 lation of VEGF/VEGFR-2 signaling, suggesting COUP-TFII as a candidate target for antiangiogenic thera
187 f COUP-TFII level in the stomach, suggesting COUP-TFII as a target of hedgehog signaling in the stoma
188 nto a life-threatening disease, and supports COUP-TFII as a potential drug target for the interventio
189  the murine model, suggesting that targeting COUP-TFII is a potential treatment for DMD.
190 e in human breast cancer cell lines and that COUP-TFII plays a role in regulating the growth inhibito
191                             We conclude that COUP-TFII stimulates the transcriptional activity of the
192                  We further demonstrate that COUP-TFII directs the plasticity of mesenchymal precurso
193 Taken together, our results demonstrate that COUP-TFII plays an early role in limb bud outgrowth but
194    Taken together, our data demonstrate that COUP-TFII represents an endogenous suppressor of adipoge
195                 We further demonstrated that COUP-TFII also reduces the activation of focal adhesion
196 rotein-DNA binding studies demonstrated that COUP-TFII binds to an imperfect direct repeat COUP-TFII
197           Recently we have demonstrated that COUP-TFII expression in the hypothalamus is restricted t
198      Using ChIP assays, we demonstrated that COUP-TFII was recruited to the promoter region of IGF-1
199 ore, cotransfection assays demonstrated that COUP-TFII/ARP-1 inhibits the USF2-mediated activation of
200          Mechanistically, we determined that COUP-TFII coordinated a regenerative program through com
201            In this study, we discovered that COUP-TFII, a transcription factor critical for establish
202                                We found that COUP-TFII expression is suppressed by SCF through phosph
203                                We found that COUP-TFII functions as a coregulator of Prox1 to control
204                                We found that COUP-TFII plays a cell-autonomous role in endothelial ce
205              Thus, our results indicate that COUP-TFII regulates growth and maturation of the mouse p
206 urin transgenic mouse model, indicating that COUP-TFII may serve as a therapeutic target for the trea
207 ficient mice, which supports the notion that COUP-TFII controls Angiopoietin-1/Tie2 signaling to regu
208        Collectively, our results reveal that COUP-TFII confers atrial identity through direct binding
209     Mechanistic investigations revealed that COUP-TFII suppressed vascular endothelial growth factor
210          Mobility shift assays revealed that COUP-TFII/ARP-1 and USF2 compete for binding to the ATPA
211                           Here, we show that COUP-TFII (also known as Nr2f2), a member of the orphan
212                           Here, we show that COUP-TFII (also known as Nr2f2), an orphan member of the
213                                 We show that COUP-TFII acts downstream of hedgehog signaling and is r
214                    Importantly, we show that COUP-TFII directly regulates the expression of both Eya1
215                    Further studies show that COUP-TFII is a critical factor controlling metastatic ge
216                Altogether our data show that COUP-TFII is involved in the control of renin gene expre
217                               We showed that COUP-TFII directly regulates the transcription of Angiop
218 ure and in vivo mouse models, we showed that COUP-TFII hinders myogenic development by repressing myo
219  Functional assays in HeLa cells showed that COUP-TFII/ARP-1 represses the ATPA promoter activity in
220                      These data suggest that COUP-TFII affects mitochondrial function, impairs metabo
221 the renin gene expression, we suggested that COUP-TFII may modulate this cAMP effect.
222  of tumor lymphangiogenesis, suggesting that COUP-TFII also regulates neo-lymphangiogenesis in the ad
223 ghout embryonic development, suggesting that COUP-TFII is involved in multiple aspects of embryogenes
224                    Our finding suggests that COUP-TFII is a likely contributor to the formation of CD
225           This down-regulation suggests that COUP-TFII may be required for bidirectional signaling be
226            We report for the first time that COUP-TFII, but not COUP-TFI, is reduced in three antiest
227 ur findings reveal, for the first time, that COUP-TFII plays a central role in the specification of m
228                        However, although the COUP-TFII nuclear receptor has recently been shown to re
229 ores the angiogenic defects exhibited by the COUP-TFII-deficient mice, which supports the notion that
230  generation of a lacZ knock-in allele in the COUP-TFII locus in mice allows us to use X-gal staining
231                                       In the COUP-TFII mutant heart, the atria and sinus venosus fail
232                     Targeted deletion of the COUP-TFII gene results in embryonic lethality with defec
233 ypassed the early embryonic lethality of the COUP-TFII mutant by using two methods.
234 pecific miRNAs through the regulation of the COUP-TFII-FOXM1-CENPF cascade in PCa metastasis and drug
235          Overexpression of USF2 reversed the COUP-TFII/ARP-1-mediated repression of the ATPA promoter
236 ing conserved regulatory elements within the COUP-TFII promoter and remodeling chromatin to make the
237                                   Therefore, COUP-TFII expression levels in the ventromedial nucleus
238 XM1 and CENPF by these miRNAs occurs through COUP-TFII, a member of the orphan nuclear receptors fami
239                                        Thus, COUP-TFII has a critical role in repressing Notch signal
240                                        Thus, COUP-TFII is a critical factor that controls lymphangiog
241 ntiated by patient sample analysis, in which COUP-TFII expression or activity is tightly correlated w
242 /PCK1 is a pleiotropic element through which COUP-TFII inhibits premature PEPCK expression, and perha
243 by supershifting the corresponding band with COUP-TFII-specific antibodies.
244                                     ECs with COUP-TFII knockdown also readily undergo endothelial-to-

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