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1                                              COUP-TF bound to an ERE half-site with high affinity, Kd
2                                              COUP-TF, an orphan member of the nuclear receptor superf
3                                              COUP-TF-interacting protein 2 (CTIP2; also known as Bcl1
4                                              COUP-TFs are also involved in the regulation of several
5                                              COUP-TFs are transcription factors which have been shown
6                                              COUP-TFs bind to a site between the two Smad binding ele
7 s modulators of the activity of NR2F1 and 2 (COUP-TFs), which are orphan NHRs that are critical for d
8 not remodel, the transcription factor UNC-55/COUP-TF turns off IRX-1, thus maintaining high levels of
9 DD neurons but is repressed in VDs by UNC-55/COUP-TF.
10                                            A COUP-TF-binding site was then identified within the B2 s
11 he promoter region of this gene identified a COUP-TF-responsive element between positions -64 and -46
12 robe were supershifted with antibody against COUP-TF, identifying COUP-TF as the candidate repressor
13                                     Although COUP-TFs function as potent transcription repressors, th
14 tivities and nuclear expression of Sp1/3 and COUP-TF in normal fetal mouse heart were similar to thos
15 dependent transcriptional autoactivation and COUP-TF-dependent repression.
16 functions as a corepressor for both GATA and COUP-TF proteins.
17 uilibrium between orphan receptors nur77 and COUP-TF, through their heterodimerization that regulates
18 ed COUP-TF binds to the -295/-199 region and COUP-TF represses T3-dependent activation of the PCP-2 p
19 but is through interaction between nur77 and COUP-TFs.
20 etting the balance between opposing Smad and COUP-TFs.
21           In a transient transfection assay, COUP-TF strongly induced transcriptional activity of the
22                In gel mobility shift assays, COUP-TF bound as an apparent dimer to ERE and ERE half-s
23  demonstrated a positive correlation between COUP-TF expression and the ability of trans-RA to inhibi
24 counterpart to the rodent FoxA site can bind COUP-TF factors.
25 here as RID1 and RID2) permit BCL11A to bind COUP-TFs (NR2F1;NR2F2;NR2F6) and Tailless/TLX (NR2E1), w
26 s well as potential Smad, FoxH1/FAST, T-box, COUP-TF, C/EBP, GATA, HNF3 binding sites and retinoic ac
27 stinct cell-intrinsic mechanisms mediated by COUP-TF genes to direct the specification and differenti
28 hance transcriptional repression mediated by COUP-TF II and have been implicated in hematopoietic cel
29 he transactivation of the NGFI-A promoter by COUP-TF.
30      In order to identify genes regulated by COUP-TF in this process, a rat urogenital mesenchymal ce
31 chanisms of activation of gene expression by COUP-TFs.
32 that Pax6 and Otx2 are directly regulated by COUP-TFs.
33 scription factors mediates its regulation by COUP-TFs.
34                  Substitution of a consensus COUP-TF-binding site for the c-mos negative regulatory e
35                                  In contrast COUP-TFs are transcriptional activators of PEPCK in hepa
36                                  Conversely, COUP-TF transcribed and translated in vitro enhanced the
37 hly expressed in the brain, CTIP1 and CTIP2 (COUP TF-interacting proteins 1 and 2, respectively), wer
38 ein 2)-mediated repression, increased Ctip2 (COUP-TF interacting protein 2) promoter activity, and Ct
39 s that repress transcription through direct, COUP-TF-in-dependent binding to a GC-rich response eleme
40          We provide evidence that endogenous COUP-TF activity represses the COL7A1 promoter.
41 bumin upstream promoter-transcription factor COUP-TF, pregnane X receptor (PXR), and hepatocyte nucle
42 e demonstrate here that transcription factor COUP-TF-interacting protein 1 (CTIP1/BCL11A; hereafter C
43 vered that mice lacking transcription factor COUP-TF-interacting protein 2 (Ctip2) exhibit EPB defect
44 umin upstream promoter-transcription factor (COUP-TF) 2 and COUP-TF3.
45 umin upstream promoter transcription factor (COUP-TF) binds specifically to AF3 and that upstream sti
46 ding site for the COUP transcription factor (COUP-TF) is also required for Ov gene transcription.
47 umin upstream promoter-transcription factor (COUP-TF) plays a role in mediating the growth inhibitory
48 umin upstream promoter-transcription factor (COUP-TF) represses triiodothyronine (T3)-dependent trans
49 umin upstream promoter-transcription factor (COUP-TF) subfamily of orphan nuclear receptors, which mi
50 umin upstream promoter transcription factor (COUP-TF) subfamily of orphan nuclear receptors.
51 umin upstream promoter-transcription factor (COUP-TF) was identified as a low abundance protein in bo
52 umin upstream promoter transcription factor (COUP-TF), a nuclear orphan receptor belonging to the ste
53 umin upstream promoter transcription factor (COUP-TF), repressed transcription via the gammaRXRE.
54 umin upstream promoter transcription factor (COUP-TF)-I interacts directly with 4-hydroxytamoxifen (4
55 umin upstream promoter transcription factor (COUP-TF)-interacting protein 2 (Ctip2) knockout mice hav
56 umin upstream promoter transcription factor (COUP-TF)-interacting protein 2 (CTIP2), also known as Bc
57 umin upstream promoter transcription factor (COUP-TF)-interacting proteins 1 and 2 (CTIP1 and CTIP2)
58 umin upstream promoter transcription factor (COUP-TF)-mediated transcriptional repression.
59 umin upstream promoter transcription factor (COUP-TF).
60 umin upstream promoter transcription factor (COUP-TF)/erbA-related protein 3] families interact with
61 min upstream promoter-transcription factors (COUP-TFs), orphan members of the nuclear receptor superf
62 two functionally distinct accessory factors, COUP-TF/HNF4 and HNF3, respectively.
63 ted from -130 to -100 and designated CAR for COUP-TF adjacent repressor.
64 ssays, we show that the region necessary for COUP-TF silencing function is not sufficient for its tra
65 lts suggest that NGFI-A is a target gene for COUP-TFs and that the Sp1 family of transcription factor
66  addition to its active repression function, COUP-TF can repress several different types of activator
67  In the mouse, there are two very homologous COUP-TF genes (I and II) and their expression patterns o
68 n Strongylocentrotus purpuratus with a human COUP-TF I cDNA probe revealed the presence of a novel ge
69  Deletion of the DNA-binding domain of human COUP-TF I resulted in loss of all aspects of nuclear per
70                         The pattern of human COUP-TF I subcellular localization, detected with a mono
71 subcellular localization of myc-tagged human COUP-TF I introduced into the sea urchin embryo by RNA i
72 d with antibody against COUP-TF, identifying COUP-TF as the candidate repressor previously detected i
73 In addition, stable expression of COUP-TF in COUP-TF-negative cancer cells restores induction of RARb
74 RARs), since stable expression of COUP-TF in COUP-TF-negative HT-1376 bladder cancer cells, which do
75              Stable expression of COUP-TF in COUP-TF-negative MDA-MB231 breast cancer cells restored
76 tion domain, are also required for increased COUP-TF binding to the R2 element and decreased NF-kappa
77 ation of class I transcription by increasing COUP-TF repressor binding and decreasing NF-kappaB activ
78       The nature of the ER ligand influenced COUP-TF-ERE half-site binding.
79 of reported apo A1 transcriptional inhibitor COUP-TF, which competes with HNF4 for DNA binding.
80             In human lung cancer cell lines, COUP-TF is highly expressed in RA-sensitive cell lines w
81                                    Moreover, COUP-TF can transrepress the ligand-dependent activation
82                                     Multiple COUP-TF members have been cloned and they share a high d
83 e Sp1 family of transcription factors but no COUP-TF binding site.
84 eoproteins could be the orphan nucleoprotein COUP-TF.
85                               The ability of COUP-TF to bind specifically to EREs and half-sites, to
86 ther hand, relieves the repressive action of COUP-TF, resulting in the induction of the HGF promoter.
87 ls, demonstrating the functional activity of COUP-TF as a repressor of c-mos transcription.
88 ro studies demonstrated that the addition of COUP-TF inhibited c-Jun DNA binding through a direct pro
89    Mutations of AF3 that diminish binding of COUP-TF reduce the glucocorticoid response, but mutation
90                               The binding of COUP-TF to the DR-8 element synergistically increases th
91    This action is mediated by the binding of COUP-TF to the glucocorticoid accessory factor 1 (gAF1)
92 hat is mediated by the DNA binding domain of COUP-TF and the leucine zipper of c-Jun.
93                                The effect of COUP-TF in enhancing the trans-RA-induced antagonism of
94 rans-RA activity, we evaluated the effect of COUP-TF on antagonism of AP-1 activity by trans-RA.
95  analysis, we demonstrate that the effect of COUP-TF requires its binding to a DR-8 element present i
96 ereas inhibition of COUP-TF by expression of COUP-TF antisense RNA represses the RA effects.
97                                Expression of COUP-TF correlates with RARbeta induction in a variety o
98            In addition, stable expression of COUP-TF in COUP-TF-negative cancer cells restores induct
99 receptors (RARs), since stable expression of COUP-TF in COUP-TF-negative HT-1376 bladder cancer cells
100                         Stable expression of COUP-TF in COUP-TF-negative MDA-MB231 breast cancer cell
101                         Stable expression of COUP-TF in nur77-positive, RA-resistant lung cancer cell
102                    Conversely, expression of COUP-TF sensitizes RA responsiveness of RAREs by repress
103  transient transfection assay, expression of COUP-TF strongly inhibited tumor promoter 12-O-tetradeca
104 trategy to examine the silencing function of COUP-TF in a heterodimeric context.
105  the intrinsic active repression function of COUP-TF is not affected by heterodimerization.
106  However, this active repression function of COUP-TF may be differentially regulated by some other ac
107 , and apoptosis by RA, whereas inhibition of COUP-TF by expression of COUP-TF antisense RNA represses
108 urs in solution and results in inhibition of COUP-TF RARE binding and transcriptional activity.
109                        Direct interaction of COUP-TF with ER was indicated by GST "pull-down" and co-
110 uses a rapid and profound down-regulation of COUP-TF expression in keratinocytes and fibroblasts.
111  insights into the molecular mechanism(s) of COUP-TF-mediated repression.
112                         Unlike the effect of COUP-TFs, the function of nur77 does not require direct
113 2 rat brain extract indicate the presence of COUP-TFs, EAR2, and NURR1 in the DNA-protein complex.
114 the antiestrogen 4-hydroxytamoxifen (4-OHT), COUP-TF-half-site interaction decreased.
115            Complexes formed between purified COUP-TFs and the c-mos B2 probe comigrated in electropho
116 udies identified the orphan nuclear receptor COUP-TF as one of the endogenous cardiac proteins which
117 dy, we provide evidence that orphan receptor COUP-TF is required for induction of RARbeta expression,
118                        The nuclear receptor, COUP-TF, binds to the C2 site.
119 ough their heterodimerization that regulates COUP-TF RARE binding, is critical for RA responsiveness
120 d through increased binding of the repressor COUP-TF to the R2 element and decreased binding of the a
121 ong binding to the transcriptional repressor COUP-TF, suggest that the class I enhancer is globally d
122          First, as we have previously shown, COUP-TF is required as an accessory factor for the compl
123  inhibit E2-induced gene expression suggests COUP-TF regulates ER action by both direct DNA binding c
124 omyocyte transfection studies confirmed that COUP-TF repressed the transcriptional activity of the MC
125               These results demonstrate that COUP-TF, by serving as an accessory protein for RARalpha
126                Finally, we demonstrated that COUP-TF can directly interact with Sp1.
127 The results of these experiments reveal that COUP-TF and Oct-1 binding does not play a functional rol
128 lly, immunohistochemical studies reveal that COUP-TF is specifically expressed in the immature fetal
129     Cotransfection experiments revealed that COUP-TF and RXRalpha compete at the gammaRXRE to modulat
130 ifferentiation of progenitor cells, and that COUP-TFs are crucial for dorsalization of the eye.
131 m their expression pattern, we proposed that COUP-TFs regulate paracrine signals important for mesenc
132 ditional knockout mouse models suggests that COUP-TFs compensate for each other to maintain morphogen
133 entral D (VD) GABAergic motor neurons by the COUP-TF (chicken ovalbumin upstream promoter transcripti
134 ted that the RA response is regulated by the COUP-TF orphan receptors.
135                           Two regions of the COUP-TF molecule are shown to be important for NGFI-A ac
136 of FOG-2 and to the carboxyl terminus of the COUP-TF proteins.
137 hat has been suggested to be a member of the COUP-TF subfamily.
138 vitamin D receptor, were constituents of the COUP-TF.DNA binding complex detected in gel mobility shi
139 gen receptor gamma, which are related to the COUP-TF proteins.
140                                          The COUP-TFs are highly expressed in the developing nervous
141                                          The COUP-TFs are orphan members of the steroid/thyroid hormo
142                                        Thus, COUP-TF, through its physical interaction with AP-1, pro
143 port of this hypothesis, in vitro translated COUP-TF binds to the -295/-199 region and COUP-TF repres
144 erved sea urchin homologue of the vertebrate COUP-TFs and the Drosophila seven up subfamily of transc
145 nsight into the molecular mechanism by which COUP-TF regulates trans-RA activity, we evaluated the ef
146 to the promoter template by interaction with COUP-TF family members.
147 r77 is not required for its interaction with COUP-TF.

 
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