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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 not remodel, the transcription factor UNC-55/COUP-TF turns off IRX-1, thus maintaining high levels of
10 he promoter region of this gene identified a COUP-TF-responsive element between positions -64 and -46
11 robe were supershifted with antibody against COUP-TF, identifying COUP-TF as the candidate repressor
13 tivities and nuclear expression of Sp1/3 and COUP-TF in normal fetal mouse heart were similar to thos
16 uilibrium between orphan receptors nur77 and COUP-TF, through their heterodimerization that regulates
17 ed COUP-TF binds to the -295/-199 region and COUP-TF represses T3-dependent activation of the PCP-2 p
22 demonstrated a positive correlation between COUP-TF expression and the ability of trans-RA to inhibi
24 here as RID1 and RID2) permit BCL11A to bind COUP-TFs (NR2F1;NR2F2;NR2F6) and Tailless/TLX (NR2E1), w
25 s well as potential Smad, FoxH1/FAST, T-box, COUP-TF, C/EBP, GATA, HNF3 binding sites and retinoic ac
26 stinct cell-intrinsic mechanisms mediated by COUP-TF genes to direct the specification and differenti
27 hance transcriptional repression mediated by COUP-TF II and have been implicated in hematopoietic cel
36 hly expressed in the brain, CTIP1 and CTIP2 (COUP TF-interacting proteins 1 and 2, respectively), wer
37 ein 2)-mediated repression, increased Ctip2 (COUP-TF interacting protein 2) promoter activity, and Ct
38 s that repress transcription through direct, COUP-TF-in-dependent binding to a GC-rich response eleme
40 bumin upstream promoter-transcription factor COUP-TF, pregnane X receptor (PXR), and hepatocyte nucle
41 e demonstrate here that transcription factor COUP-TF-interacting protein 1 (CTIP1/BCL11A; hereafter C
42 vered that mice lacking transcription factor COUP-TF-interacting protein 2 (Ctip2) exhibit EPB defect
44 umin upstream promoter transcription factor (COUP-TF) binds specifically to AF3 and that upstream sti
45 ding site for the COUP transcription factor (COUP-TF) is also required for Ov gene transcription.
46 umin upstream promoter-transcription factor (COUP-TF) plays a role in mediating the growth inhibitory
47 umin upstream promoter-transcription factor (COUP-TF) represses triiodothyronine (T3)-dependent trans
48 umin upstream promoter-transcription factor (COUP-TF) subfamily of orphan nuclear receptors, which mi
50 umin upstream promoter-transcription factor (COUP-TF) was identified as a low abundance protein in bo
51 umin upstream promoter transcription factor (COUP-TF), a nuclear orphan receptor belonging to the ste
52 umin upstream promoter transcription factor (COUP-TF), repressed transcription via the gammaRXRE.
53 umin upstream promoter transcription factor (COUP-TF)-I interacts directly with 4-hydroxytamoxifen (4
54 umin upstream promoter transcription factor (COUP-TF)-interacting protein 2 (Ctip2) knockout mice hav
55 umin upstream promoter transcription factor (COUP-TF)-interacting protein 2 (CTIP2), also known as Bc
56 umin upstream promoter transcription factor (COUP-TF)-interacting proteins 1 and 2 (CTIP1 and CTIP2)
59 umin upstream promoter transcription factor (COUP-TF)/erbA-related protein 3] families interact with
60 min upstream promoter-transcription factors (COUP-TFs), orphan members of the nuclear receptor superf
63 ssays, we show that the region necessary for COUP-TF silencing function is not sufficient for its tra
64 lts suggest that NGFI-A is a target gene for COUP-TFs and that the Sp1 family of transcription factor
65 addition to its active repression function, COUP-TF can repress several different types of activator
66 In the mouse, there are two very homologous COUP-TF genes (I and II) and their expression patterns o
67 n Strongylocentrotus purpuratus with a human COUP-TF I cDNA probe revealed the presence of a novel ge
68 Deletion of the DNA-binding domain of human COUP-TF I resulted in loss of all aspects of nuclear per
70 subcellular localization of myc-tagged human COUP-TF I introduced into the sea urchin embryo by RNA i
71 d with antibody against COUP-TF, identifying COUP-TF as the candidate repressor previously detected i
72 In addition, stable expression of COUP-TF in COUP-TF-negative cancer cells restores induction of RARb
73 RARs), since stable expression of COUP-TF in COUP-TF-negative HT-1376 bladder cancer cells, which do
75 tion domain, are also required for increased COUP-TF binding to the R2 element and decreased NF-kappa
76 ation of class I transcription by increasing COUP-TF repressor binding and decreasing NF-kappaB activ
85 ther hand, relieves the repressive action of COUP-TF, resulting in the induction of the HGF promoter.
87 ro studies demonstrated that the addition of COUP-TF inhibited c-Jun DNA binding through a direct pro
88 Mutations of AF3 that diminish binding of COUP-TF reduce the glucocorticoid response, but mutation
90 This action is mediated by the binding of COUP-TF to the glucocorticoid accessory factor 1 (gAF1)
94 analysis, we demonstrate that the effect of COUP-TF requires its binding to a DR-8 element present i
98 receptors (RARs), since stable expression of COUP-TF in COUP-TF-negative HT-1376 bladder cancer cells
102 transient transfection assay, expression of COUP-TF strongly inhibited tumor promoter 12-O-tetradeca
105 However, this active repression function of COUP-TF may be differentially regulated by some other ac
106 , and apoptosis by RA, whereas inhibition of COUP-TF by expression of COUP-TF antisense RNA represses
109 uses a rapid and profound down-regulation of COUP-TF expression in keratinocytes and fibroblasts.
112 2 rat brain extract indicate the presence of COUP-TFs, EAR2, and NURR1 in the DNA-protein complex.
115 udies identified the orphan nuclear receptor COUP-TF as one of the endogenous cardiac proteins which
116 dy, we provide evidence that orphan receptor COUP-TF is required for induction of RARbeta expression,
118 ough their heterodimerization that regulates COUP-TF RARE binding, is critical for RA responsiveness
119 d through increased binding of the repressor COUP-TF to the R2 element and decreased binding of the a
120 ong binding to the transcriptional repressor COUP-TF, suggest that the class I enhancer is globally d
122 inhibit E2-induced gene expression suggests COUP-TF regulates ER action by both direct DNA binding c
123 omyocyte transfection studies confirmed that COUP-TF repressed the transcriptional activity of the MC
126 The results of these experiments reveal that COUP-TF and Oct-1 binding does not play a functional rol
127 lly, immunohistochemical studies reveal that COUP-TF is specifically expressed in the immature fetal
128 Cotransfection experiments revealed that COUP-TF and RXRalpha compete at the gammaRXRE to modulat
130 m their expression pattern, we proposed that COUP-TFs regulate paracrine signals important for mesenc
131 ditional knockout mouse models suggests that COUP-TFs compensate for each other to maintain morphogen
132 entral D (VD) GABAergic motor neurons by the COUP-TF (chicken ovalbumin upstream promoter transcripti
137 vitamin D receptor, were constituents of the COUP-TF.DNA binding complex detected in gel mobility shi
142 port of this hypothesis, in vitro translated COUP-TF binds to the -295/-199 region and COUP-TF repres
143 erved sea urchin homologue of the vertebrate COUP-TFs and the Drosophila seven up subfamily of transc
144 nsight into the molecular mechanism by which COUP-TF regulates trans-RA activity, we evaluated the ef
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