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 We then identified a VDRE cluster in the HBV core promoter that is highly con

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

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

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

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

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

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

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

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

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

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

16 nd the arginine vasopressin receptor contain VDREs for activation.

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

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

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

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

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

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

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

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

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

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

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

28 ccurring at the calcitriol response element (VDRE).

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

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

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

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

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

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

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

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

37 y genes through vitamin D response elements (VDREs) in their promoters.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

58 25-(OH)2D3 dramatically enhances heterodimer-VDRE interaction, whereas somewhat higher concentrations

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

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

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

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

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

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

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

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

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

68 key determinant of the temporal patterns of VDRE occupancy.

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

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

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

72 iated ligand-dependent transcription on only VDREs.

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

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

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

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

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

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

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

80 imers compete for binding at the osteocalcin VDRE.

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

82 at was insensitive to competition with other VDRE sequences.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

97 The VDRE binding function of VDR has been primarily ascribed

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

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

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

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

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

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

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

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

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

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

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

109 double-strand oligonucleotides harboring the VDRE.

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

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

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

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

114 3-stimulated transcriptional activity of the VDRE promoter and the expression of involucrin and CYP24

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

116 organization is abrogated by mutation of the VDRE.

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

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

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

120 tricular cardiomyocytes by Irx4 requires the VDRE.

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

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

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

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

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

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

127 25(OH)(2)D(3) induced VDR/RXR binding to the VDRE-containing proximal promoter, the VDR/RXR heterodim

128 lated the binding of nuclear proteins to the VDRE.

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

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

131 showed that VDR interacts directly with the VDRE cluster in the HBV core promoter independent of ret

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

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

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

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

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

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

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

139 Disruption of this VDRE cluster abrogated calcitriol-mediated suppression o

140 ,25(OH)(2)D(3) activation, VDR bound to this VDRE leading to recruitment of DRIP205 and RNA polymeras

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

142 min D-mediated regulation of viruses through VDREs in virus promoters.

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

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

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