ライフサイエンスコーパス: VDRE

1 E, was established in PC3 cells (OSE1 > AP-1/VDRE > OSE2).

2 ty in PC3 cells by binding to the OSE2, AP-1/VDRE, and OSE1 elements, respectively.

3 he cis-acting elements, OSE1, OSE2, and AP-1/VDRE, was established in PC3 cells (OSE1 > AP-1/VDRE > O

4 This CRM harbored 3 VDREs and single C/EBPbeta and RUNX2 sites.

5 It is a VDRE required for the regulation of Claudin-2 by vitamin

6 phrin expression in podocytes by acting on a VDRE in the proximal nephrin promoter.

7 the VDRE-BP1 cDNA, in wild-type cells with a VDRE-luciferase reporter resulted in significant reducti

8 , is a direct target for 1,25(OH)(2)D(3) and VDRE-BP, and functions to suppress cell proliferation in

9 )-treated osteoblasts confirmed that VDR and VDRE-BP compete for binding to the DDIT4 gene promoter.

10 n these mutants is not their ability to bind VDREs.

11 ose that do not activate transcription, bind VDREs with equal and high affinity, indicating that the

12 DNAs bearing the open reading frame for both VDRE-BPs were cloned and used to transfect wild-type, ho

13 Both VDREs bound the vitamin D receptor (VDR)-retinoid X rece

14 noids or 1,25(OH)2D3, while mutation of both VDREs essentially abolished the activity of the ligands

15 nd the arginine vasopressin receptor contain VDREs for activation.

16 utside the blood-brain barrier at a distinct VDRE.

17 Mutation of either VDRE diminished responsiveness of the -316 to -22 promot

18 ressed proteins, efficient binding to either VDRE occurs as a VDR.

19 ify a functional vitamin D response element (VDRE) 5-AGATAACAAAGGTCA-3 in the Cdx1 site of the Claudi

20 n the brain at a vitamin D response element (VDRE) and represses the transcription of TPH1 in tissues

21 via a consensus vitamin D response element (VDRE) in the CAMP promoter that was bound by the vitamin

22 re indicated the vitamin D response element (VDRE) in the human parathyroid hormone (hPTH) promoter c

23 ences within the vitamin D response element (VDRE) of the osteocalcin gene that are critical for YY1-

24 One putative VDR response element (VDRE) that was predicted to interact efficiently with VD

25 inding site, the vitamin D response element (VDRE), for a heterodimer of vitamin D receptor (VDR) and

26 on in trans as a vitamin D response element (VDRE)-binding protein.

27 ccurring at the calcitriol response element (VDRE).

28 sequences known as the VD response element (VDRE).

29 r binding to the vitamin D response element (VDRE).

30 of a functional vitamin D response element (VDRE).

31 nocytes, and a vitamin D responsive element (VDRE) in its promoter region has been identified.

32 e identified a vitamin D responsive element (VDRE) in the promoter region of the human KSR-1 gene, to

33 ls to generate vitamin D-responsive element (VDRE)-reactive nuclear protein complexes or to initiate

34 es occupancy of vitamin D response elements (VDREs) by the VDRE binding protein (VDRE-BP) or 1,25(OH)

35 BD with several vitamin D response elements (VDREs) in the absence of accessory proteins such as reti

36 d characterized vitamin D response elements (VDREs) located in both genes and showed that 1,25D treat

37 at binds to two vitamin D response elements (VDREs) located near the proximal promoter.

38 equences termed vitamin D response elements (VDREs) thereby enhancing or repressing transcription.

39 transactivating vitamin D-response elements (VDREs) within its promoter.

40 everal putative vitamin D response elements (VDREs), and EMSA confirmed that the VDRE at -312 (a DR4-

41 ny recognizable vitamin D response elements (VDREs), high affinity DNA binding by recombinant VDR is

42 eta) binding to vitamin D response elements (VDREs), two thyroid hormone response elements (TREs) (DR

43 rat osteocalcin vitamin D-response elements (VDREs).

44 ceptor (RXR) on vitamin D response elements (VDREs).

45 ously defined vitamin D-responsive elements (VDREs) at -294 to -274 and -174 to -151.

46 es, candidate vitamin D responsive elements (VDREs) at -7/-10 kb in human tryptophan hydroxylase (TPH

47 repeat (DR+3) vitamin D responsive elements (VDREs) located in target genes.

48 peratively to vitamin D responsive elements (VDREs) to activate or repress the transcription of a mul

49 This relationship is disrupted by elevated VDRE-BP, causing a form of hereditary vitamin D-resistan

50 s to effect transcriptional enhancement from VDRE-linked promoter-containing DNA.

51 RXR and VDR transactivated selectively from VDRE-linked templates exclusively as a heterodimeric com

52 el the latter was attenuated by a functional VDRE in the CYP24A1 promoter.

53 egulation was VDR-dependent and a functional VDRE in the promoter was identified.

54 The induction of the human PLC-gamma1 VDRE by 1,25(OH)2D3 was synergistic with all-trans retin

55 and SCC12B2 cells bound the human PLC-gamma1 VDRE similarly to that seen in normal keratinocytes.

56 25-(OH)2D3 dramatically enhances heterodimer-VDRE interaction, whereas somewhat higher concentrations

57 acts formed a specific complex with the hPTH VDRE that was insensitive to competition with other VDRE

58 were rendered insensitive to the hormone in VDRE-BP-overexpressing HVDRR cells.

59 equencing of tryptic peptides from a 34-kDa (VDRE-BP1) and 38-kDa species (VDRE-BP-2) possessed seque

60 To define the minimal VDRE binding domain for human VDR (hVDR), a series of C-

61 found at position -1867, as well as numerous VDRE and NFkappaB sites found throughout the promoter an

62 a-catenin and ligand-dependent activation of VDRE-containing promoters.

63 The addition of VDRE DNA, but not random DNA, caused changes in the prot

64 otein and necessary for the establishment of VDRE binding complexes and the induction of 24-hydroxyla

65 o 1,25(OH)(2)D(3), whereas overexpression of VDRE-BP exerted a dominant-negative effect on transcript

66 key determinant of the temporal patterns of VDRE occupancy.

67 caused changes in the proton NMR spectra of VDRE DNA indicating specific interaction between protein

68 this study, we demonstrated the presence of VDREs in the intronic conserved noncoding sequence regio

69 Molecular modeling and studies on VDRE-transcriptional activity excludes action through th

70 iated ligand-dependent transcription on only VDREs.

71 RXRalpha-VDR complexes were shown to bind OP VDRE.

72 e osteopontin vitamin D response element (OP VDRE).

73 on of 9-c-RA increased RXRalpha homodimer-OP VDRE complexes, and addition of 1,25-(OH) 2D3 resulted i

74 arily as monomers, but in the presence of OP VDRE, homodimeric RXRalpha and heterodimeric RXRalpha-VD

75 formation of 1, 25-(OH)2D 3-VDR-RXRalpha-OP VDRE complexes.

76 no detectable effect on the VDR-RXRalpha-OP VDRE transcription complex.

77 fic DNA-protein interactions at the OCFRE or VDRE, respectively, as detected by gel shift assay.

78 imers compete for binding at the osteocalcin VDRE.

79 the absence of ligand on DR3 and osteopontin VDREs and F2, but had no effect on DR4 or DR5.

80 at was insensitive to competition with other VDRE sequences.

81 distinct conformation relative to a positive VDRE, suggesting that the DNA element itself acts as an

82 n contrast to VDR interactions with positive VDREs, this binding is independent of VDR's heterodimeri

83 whether this downstream region and potential VDREs located within mediated CYP24A1 induction, we cons

84 vitamin D response element-binding protein (VDRE-BP) and squelching of vitamin d-directed transactiv

85 lements (VDREs) by the VDRE binding protein (VDRE-BP) or 1,25(OH)(2)D(3)-bound vitamin D receptor (VD

86 owed that VDR DBD was able to form a protein/VDRE DNA structural complex.

87 These data suggest that the hnRNPA2-related VDRE-BP2 is a dominant-negative regulator of vitamin D a

88 overned by 1,25D, potentially via respective VDREs located at -7/-10 kb and -28 kb.

89 112) in the context of the complete hVDR-RXR-VDRE interaction.

90 R, and site-directed mutagenesis of a single VDRE within this region abolished this activation.

91 several putative response elements for Sox9, VDRE, Runx and Sp1.

92 from a 34-kDa (VDRE-BP1) and 38-kDa species (VDRE-BP-2) possessed sequence homology with human hetero

93 ocation of the VDR to the nucleus, stimulate VDRE-reporter activity, regulate VDR downstream genes (V

94 ement of the FOXP3 promoter activity by such VDREs in response to 1,25(OH)(2)VD(3).

95 The VDRE binding function of VDR has been primarily ascribed

96 nscription start site of KSR-1 gene, and the VDRE is functional in reporter assays.

97 f VDR, RXR alpha, and Irx4 that binds at the VDRE inhibiting slow MyHC3 expression in the ventricles.

98 ol-regulated DNA-protein interactions at the VDRE.

99 VDR antagonists, which block the VDRE-directed activity of the VDR and recruitment of cla

100 th the interactions of the VDR with both the VDRE and TFIIB.

101 ctivation by NF-Y interactions with both the VDRE site and a previously described distal NF-Y-binding

102 the Delta134 and Delta113 mutants bound the VDRE (predominantly as monomers), suggesting that, in ad

103 f vitamin D response elements (VDREs) by the VDRE binding protein (VDRE-BP) or 1,25(OH)(2)D(3)-bound

104 romoter-luciferase constructs containing the VDRE and tested the response of these constructs to 1,25

105 stranded DNA (dsDNA) sequence containing the VDRE from the mouse osteopontin gene.

106 In contrast, the construct containing the VDRE of the human 24-hydroxylase gene was induced severa

107 double-strand oligonucleotides harboring the VDRE.

108 ggests the lack of a cofactor(s) linking the VDRE to the transcriptional machinery.

109 expression of the VDRE-BP2 cDNA, but not the VDRE-BP1 cDNA, in wild-type cells with a VDRE-luciferase

110 by competitive, reciprocal occupancy of the VDRE by hnRNP C1/C2.

111 es revealed evolutionary conservation of the VDRE in a short interspersed nuclear element or SINE in

112 3-stimulated transcriptional activity of the VDRE promoter and the expression of involucrin and CYP24

113 Transient and stable overexpression of the VDRE-BP2 cDNA, but not the VDRE-BP1 cDNA, in wild-type c

114 organization is abrogated by mutation of the VDRE.

115 tion of histones H3 and H4 downstream of the VDRE.

116 e partially overlapped the 3' portion of the VDRE.

117 cyclical movement of the VDR on and off the VDRE is legislated by competitive, reciprocal occupancy

118 tricular cardiomyocytes by Irx4 requires the VDRE.

119 in the absence of Runx2 binding but that the VDRE and vitamin D are required for enhanced acetylation

120 lements (VDREs), and EMSA confirmed that the VDRE at -312 (a DR4-type VDRE) could be bound by vitamin

121 The data indicate that the VDRE in the human PLC-gamma1 gene is not functional in S

122 uited to the OC promoter and, therefore, the VDRE is not competent to mediate vitamin D responsivenes

123 odimer competed with NF-Y for binding to the VDRE sequence, and NF-Y-stimulated activity of the hPTH

124 in VDR to a form that not only binds to the VDRE with high affinity and specificity as a heterodimer

125 25(OH)(2)D(3) induced VDR/RXR binding to the VDRE-containing proximal promoter, the VDR/RXR heterodim

126 lated the binding of nuclear proteins to the VDRE.

127 XR alpha, Irx4 does not bind directly to the VDRE.

128 moter is not significantly impaired when the VDRE is mutated.

129 n of VDR and hnRNPC1/C2 interaction with the VDRE was lost in HVDRR cells overexpressing the hnRNP C1

130 Heterologous promoter vectors driven by the VDREs were responsive to a retinoid X receptor (RXR)-sel

131 fic regulation of immunity by vitamin D, the VDREs are present in primate genes, but neither the VDRE

132 re present in primate genes, but neither the VDREs nor the regulation by 1,25D is present in mice.

133 VDR/RXR bound well to the VDREs and to DR4 and DR5 using the electrophoretic mobil

134 eptor, RAR, or RXR alone did not bind to the VDREs; however, the combination of either vitamin D rece

135 This VDRE served as a strong binding site for the recombinant

136 ,25(OH)(2)D(3) activation, VDR bound to this VDRE leading to recruitment of DRIP205 and RNA polymeras

137 ) from the vitamin D receptor (VDR) on those VDREs.

138 confirmed that the VDRE at -312 (a DR4-type VDRE) could be bound by vitamin D receptor (VDR)/retinoi

139 s for both hnRNPC1 and hnRNPC2 inhibited VDR-VDRE-directed transactivation (28 and 43%, respectively;

140 y to purify proteins associated with non-VDR-VDRE binding activity from vitamin d-resistant New World