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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
8 DD neurons but is repressed in VDs by UNC-55/COUP-TF.
9                                            A COUP-TF-binding site was then identified within the B2 s
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
12                                     Although COUP-TFs function as potent transcription repressors, th
13 tivities and nuclear expression of Sp1/3 and COUP-TF in normal fetal mouse heart were similar to thos
14 dependent transcriptional autoactivation and COUP-TF-dependent repression.
15 functions as a corepressor for both GATA and COUP-TF proteins.
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
18 but is through interaction between nur77 and COUP-TFs.
19 etting the balance between opposing Smad and COUP-TFs.
20           In a transient transfection assay, COUP-TF strongly induced transcriptional activity of the
21                In gel mobility shift assays, COUP-TF bound as an apparent dimer to ERE and ERE half-s
22  demonstrated a positive correlation between COUP-TF expression and the ability of trans-RA to inhibi
23 counterpart to the rodent FoxA site can bind COUP-TF factors.
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
28 he transactivation of the NGFI-A promoter by COUP-TF.
29      In order to identify genes regulated by COUP-TF in this process, a rat urogenital mesenchymal ce
30 chanisms of activation of gene expression by COUP-TFs.
31 that Pax6 and Otx2 are directly regulated by COUP-TFs.
32 scription factors mediates its regulation by COUP-TFs.
33                  Substitution of a consensus COUP-TF-binding site for the c-mos negative regulatory e
34                                  In contrast COUP-TFs are transcriptional activators of PEPCK in hepa
35                                  Conversely, COUP-TF transcribed and translated in vitro enhanced the
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
39          We provide evidence that endogenous COUP-TF activity represses the COL7A1 promoter.
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
43 umin upstream promoter-transcription factor (COUP-TF) 2 and COUP-TF3.
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
49 umin upstream promoter transcription factor (COUP-TF) subfamily of orphan nuclear receptors.
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)
57 umin upstream promoter transcription factor (COUP-TF)-mediated transcriptional repression.
58 umin upstream promoter transcription factor (COUP-TF).
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
61 two functionally distinct accessory factors, COUP-TF/HNF4 and HNF3, respectively.
62 ted from -130 to -100 and designated CAR for COUP-TF adjacent repressor.
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
69                         The pattern of human COUP-TF I subcellular localization, detected with a mono
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
74              Stable expression of COUP-TF in COUP-TF-negative MDA-MB231 breast cancer cells restored
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
77       The nature of the ER ligand influenced COUP-TF-ERE half-site binding.
78 of reported apo A1 transcriptional inhibitor COUP-TF, which competes with HNF4 for DNA binding.
79             In human lung cancer cell lines, COUP-TF is highly expressed in RA-sensitive cell lines w
80                                    Moreover, COUP-TF can transrepress the ligand-dependent activation
81                                     Multiple COUP-TF members have been cloned and they share a high d
82 e Sp1 family of transcription factors but no COUP-TF binding site.
83 eoproteins could be the orphan nucleoprotein COUP-TF.
84                               The ability of COUP-TF to bind specifically to EREs and half-sites, to
85 ther hand, relieves the repressive action of COUP-TF, resulting in the induction of the HGF promoter.
86 ls, demonstrating the functional activity of COUP-TF as a repressor of c-mos transcription.
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
89                               The binding of COUP-TF to the DR-8 element synergistically increases th
90    This action is mediated by the binding of COUP-TF to the glucocorticoid accessory factor 1 (gAF1)
91 hat is mediated by the DNA binding domain of COUP-TF and the leucine zipper of c-Jun.
92                                The effect of COUP-TF in enhancing the trans-RA-induced antagonism of
93 rans-RA activity, we evaluated the effect of COUP-TF on antagonism of AP-1 activity by trans-RA.
94  analysis, we demonstrate that the effect of COUP-TF requires its binding to a DR-8 element present i
95 ereas inhibition of COUP-TF by expression of COUP-TF antisense RNA represses the RA effects.
96                                Expression of COUP-TF correlates with RARbeta induction in a variety o
97            In addition, stable expression of COUP-TF in COUP-TF-negative cancer cells restores induct
98 receptors (RARs), since stable expression of COUP-TF in COUP-TF-negative HT-1376 bladder cancer cells
99                         Stable expression of COUP-TF in COUP-TF-negative MDA-MB231 breast cancer cell
100                         Stable expression of COUP-TF in nur77-positive, RA-resistant lung cancer cell
101                    Conversely, expression of COUP-TF sensitizes RA responsiveness of RAREs by repress
102  transient transfection assay, expression of COUP-TF strongly inhibited tumor promoter 12-O-tetradeca
103 trategy to examine the silencing function of COUP-TF in a heterodimeric context.
104  the intrinsic active repression function of COUP-TF is not affected by heterodimerization.
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
107 urs in solution and results in inhibition of COUP-TF RARE binding and transcriptional activity.
108                        Direct interaction of COUP-TF with ER was indicated by GST "pull-down" and co-
109 uses a rapid and profound down-regulation of COUP-TF expression in keratinocytes and fibroblasts.
110  insights into the molecular mechanism(s) of COUP-TF-mediated repression.
111                         Unlike the effect of COUP-TFs, the function of nur77 does not require direct
112 2 rat brain extract indicate the presence of COUP-TFs, EAR2, and NURR1 in the DNA-protein complex.
113 the antiestrogen 4-hydroxytamoxifen (4-OHT), COUP-TF-half-site interaction decreased.
114            Complexes formed between purified COUP-TFs and the c-mos B2 probe comigrated in electropho
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,
117                        The nuclear receptor, COUP-TF, binds to the C2 site.
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
121          First, as we have previously shown, COUP-TF is required as an accessory factor for the compl
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
124               These results demonstrate that COUP-TF, by serving as an accessory protein for RARalpha
125                Finally, we demonstrated that COUP-TF can directly interact with Sp1.
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
129 ifferentiation of progenitor cells, and that COUP-TFs are crucial for dorsalization of the eye.
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
133 ted that the RA response is regulated by the COUP-TF orphan receptors.
134                           Two regions of the COUP-TF molecule are shown to be important for NGFI-A ac
135 of FOG-2 and to the carboxyl terminus of the COUP-TF proteins.
136 hat has been suggested to be a member of the COUP-TF subfamily.
137 vitamin D receptor, were constituents of the COUP-TF.DNA binding complex detected in gel mobility shi
138 gen receptor gamma, which are related to the COUP-TF proteins.
139                                          The COUP-TFs are highly expressed in the developing nervous
140                                          The COUP-TFs are orphan members of the steroid/thyroid hormo
141                                        Thus, COUP-TF, through its physical interaction with AP-1, pro
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
145 to the promoter template by interaction with COUP-TF family members.
146 r77 is not required for its interaction with COUP-TF.

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