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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
25 ologic studies show that in L35 cells, ARP-1/COUP-TFII is bound to the DR1 element, whereas in FAO ce
28 ream promoter transcription factor II (ARP-1/COUP-TFII) and retinoid X receptor (RXRalpha) as the pro
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
39 unctional link between hedgehog proteins and COUP-TFII, factors that are vital for epithelial-mesench
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
47 erial markers whereas venous markers such as COUP-TFII are normally expressed, suggesting that mutant
51 ruction of the TGF-beta-dependent barrier by COUP-TFII is crucial for the progression of PTEN-mutant
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
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
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
66 nerated a mouse model ectopically expressing COUP-TFII in myogenic precursors to maintain COUP-TFII a
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
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
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
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
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
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
98 ll culture studies, mutant mice deficient in COUP-TFII have lower renin expression than their control
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
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.
123 et factor that is required for activation of COUP-TFII-, Islet1-, and Gli response element-dependent
126 ortant question of whether downregulation of COUP-TFII expression is required for proper muscle cell
128 amine treatment, we showed downregulation of COUP-TFII level in the stomach, suggesting COUP-TFII as
130 show an age-related decline in expression of COUP-TFII in human fetal LC, this mechanism may also be
136 To analyze the physiological function of COUP-TFII during organogenesis, we used the cre/loxP sys
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
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
147 we show that tissue-specific null mutants of COUP-TFII exhibit Bochdalek-type CDH, the most common fo
152 genesis, whereas shRNA-mediated reduction of COUP-TFII promotes differentiation, as shown by increase
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
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
162 Specifically, we found that suppression of COUP-TFII in venous ECs switched its phenotype toward pr
165 al role in induction of arterial phenotypes, COUP-TFII is required to maintain the venous EC identity
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
171 origenesis to show that the nuclear receptor COUP-TFII is essential to regulate the balance between p
173 Binding of the orphan nuclear receptor, COUP-TFII/ARP-1, to the ATPA regulatory element 1 was co
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
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
190 e in human breast cancer cell lines and that COUP-TFII plays a role in regulating the growth inhibito
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
196 rotein-DNA binding studies demonstrated that COUP-TFII binds to an imperfect direct repeat COUP-TFII
199 ore, cotransfection assays demonstrated that COUP-TFII/ARP-1 inhibits the USF2-mediated activation of
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
209 Mechanistic investigations revealed that COUP-TFII suppressed vascular endothelial growth factor
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
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
227 ur findings reveal, for the first time, that COUP-TFII plays a central role in the specification of m
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
234 pecific miRNAs through the regulation of the COUP-TFII-FOXM1-CENPF cascade in PCa metastasis and drug
236 ing conserved regulatory elements within the COUP-TFII promoter and remodeling chromatin to make the
238 XM1 and CENPF by these miRNAs occurs through COUP-TFII, a member of the orphan nuclear receptors fami
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
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