ライフサイエンスコーパス: VDR

1 VDR 4-1 also effectively suppressed secondary hyperparat

2 VDR and RXR expression were assessed by immunohistochemi

3 VDR haplotypes are associated with breast cancer in Afri

4 VDR modifies gene expression by binding DNA as a heterod

5 VDR polymorphisms (rs1544410, rs10735810, rs7975232, rs1

6 VDR polymorphisms (Taq-I, Bsm-I, Apa-I and Fok-I) were i

7 VDR-BVs are enriched in consensus RXR::VDR binding motif

8 VDR-mediated up-regulation of Mmp13 transcription was co

9 VDR-null (VDR(-/-)) mice exhibit lack of postmorphogenic

10 nificantly varied according to genotype at 2 VDR SNPs (rs7968585 and rs731236) in linkage disequilibr

11 s in part address the ability of 1,25(OH)2D3-VDR to inhibit EAE.

12 Finally, we compared 341 VDR-BVs replicating by position in multiple individuals

13 (95% CI): VDR >/= median = 0.67 (0.48-0.93); VDR < median = 0.98 (0.72-1.35), P heterogeneity = 0.12]

14 VDR genotype/haplotype, and after applying a VDR genotype-25-OHD interaction term.

15 rated potent transcriptional activities in a VDR reporter gene assay, and significantly ameliorated c

16 ry and vasodilatory mediator production in a VDR-dependent manner in vitro.

17 Neither a VDR agonist (VDA) nor an HDAC inhibitor (HDACI) nor a de

18 t 1,25D regulates DMP-1 expression through a VDR-dependent mechanism, possibly contributing to local

19 decreased Claudin-2 expression by abolishing VDR/promoter binding.

20 of the gene promoter, occupied by activated VDR and prebound C/EBPbeta and RUNX2, respectively.

21 ssociated with altered VDR binding affinity (VDR-BVs) using a high-resolution (ChIP-exo) genome-wide

22 citriol), a naturally occurring VDR agonist, VDR 4-1 therapy even at high doses did not induce hyperc

23 riants significantly associated with altered VDR binding affinity (VDR-BVs) using a high-resolution (

24 Moreover, TGF-beta and VDR signaling and CD44 splicing pathways associated with

25 mans identified SNPs in IL4, DEFB1, CRP, and VDR for persistent nasal carriage.

26 An epistatic effect between CYP11A1 and VDR polymorphisms may contribute to the predisposition t

27 Combining carriers of A allele in CYP2R1 and VDR genes with IL28B C/C genotype increased the probabil

28 CYP2R1 and VDR haplotypes altered eczema susceptibility and eosinop

29 Vitamin D and VDR may have a combined role in IA development in childr

30 n was found between Claudin-2 expression and VDR and TGR5 expression.

31 ated genes (CYP27A1, CYP2R1, CYP27B1, GC and VDR) were genotyped in 1442 Chinese children with eczema

32 served interactions between 25-OHD level and VDR genotype, suggesting a causal relationship between v

33 Genetic polymorphisms of MMP3 and VDR are linked to initial periodontitis in Finnish adole

34 cers, a region proximal to the promoter, and VDR or RUNX2.

35 equivalently in chimeras with wild type and VDR BM.

36 nificant decreased Claudin-2 in VDR(-/-) and VDR(DeltaIEC) mice.

37 4A1 and CYP27B1 protein expression in WT and VDR KO cells, and stimulated cell proliferation in both

38 biota raised serum IgE 4-fold in both WT and VDR KO mice.

39 nction, RNA sequencing of wild-type (WT) and VDR(-/-) KSCs was performed.

40 A lead compound (known as VDR 4-1) demonstrated potent transcriptional activities

41 Vitamin D deficient, VDR KO, and B-VDR KO mice developed hyper-IgE, whereas T-VDR KO mice d

42 nteric lymph node cultures from VDR KO and B-VDR KO mice secreted higher IgE ex vivo than wild-type (

43 VDR KO mice was 2-fold greater than in the B-VDR KO mice, suggesting that VDR deficiency in non-B cel

44 cific VDR (T-VDR) KO, B cell-specific VDR (B-VDR) KO, and vitamin D deficient mice were used to deter

45 d to determine degree of association between VDR polymorphisms and periodontal status adjusted for kn

46 No relation was found between VDR rs1544410CT, ADAR rs1127309TC, OASL rs1169279CT poly

47 eptor (VDR), enabling an interaction between VDR and the coactivator, SRC-3 (NCOA3), thereby increasi

48 al effects of VDR, indicating a link between VDR and PPARgamma signaling in regulating both vitamin D

49 ted the difference in IgE production between VDR KO and WT cultures.

50 Using whole body VDR(-/-) mice, intestinal epithelial VDR conditional kno

51 Whole-body VDR KO, T cell-specific VDR (T-VDR) KO, B cell-specific

52 ly one of the bone cell-type enhancers bound VDR in kidney tissue, and none were occupied by the VDR

53 e repression of fibrosis and inflammation by VDR agonists.

54 o vitamin D supplementation is influenced by VDR polymorphisms, specifically for carriers of Taq-I GG

55 s for modulating gene regulation mediated by VDR.

56 d not find clear evidence of modification by VDR variants.

57 Moreover, this association was modified by VDR rs7975232 (interaction P = 0.0072), where increased

58 reveals the binding of two LCA molecules by VDR.

59 um ASBT and decreased liver IL-10, FXR, CAR, VDR, BSEP, MRP2, MRP3, MRP4 was also observed in ANIT-in

60 pport the conclusion that absent immune cell VDR expression (a) does not impact the strength, phenoty

61 D-1alpha-hydroxylase (CYP27B1) and mast cell-VDR activity.

62 response that required functional mast cell-VDRs and mast cell-CYP27B1.

63 , we hypothesized that activation of central VDR links vitamin D to the regulation of glucose and ene

64 VDR [>/=30 ng/mL vs. <30 ng/mL RR (95% CI): VDR >/= median = 0.67 (0.48-0.93); VDR < median = 0.98 (

65 Combining VDR rs2228570 A/A genotype with IL28B C/C genotype incre

66 thally irradiated C57BL/6 mice with congenic VDR or wild type BM.

67 ship between the oncogene Ras, the vitamin D/VDR axis and the expression of DNA repair factors, in th

68 DR) during OIS, and a role for the vitamin D/VDR axis regulating the levels of these DNA repair facto

69 Vitamin D deficient, VDR KO, and B-VDR KO mice developed hyper-IgE, whereas T

70 -dependent and vitamin D receptor-dependent (VDR-dependent) pathways, respectively.

71 ses demonstrated that these genes are direct VDR targets in WT keratinocytes.

72 CRM) at -28 kb that 1,25D-dependently docked VDR, RXR, C/EBPbeta, and RUNX2.

73 le body VDR(-/-) mice, intestinal epithelial VDR conditional knockout (VDR(DeltaIEC)) mice, and cultu

74 Especially VDR target genes CYP24A1, IGFBP-3, and TRPV6 were negati

75 estimated interactions between sun exposure, VDR variants, and breast cancer in a nested case-control

76 with mast cells that did or did not express VDR or CYP27B1.

77 a direct target of the transcription factor VDR.

78 GW0742 is the first VDR ligand inhibitor lacking the secosteroid structure o

79 ir heterodimerization, which is critical for VDR:RXR target gene recruitment.

80 ition of two ligand molecules is crucial for VDR agonism by LCA.

81 antagonist activity for GW0742 was found for VDR and the androgen receptor.

82 reveals an important and novel mechanism for VDR by regulation of epithelial barriers.

83 tal long bone length may indicate a role for VDR in fetal bone development, potentially by mediating

84 tional mutagenesis defined binding sites for VDR and RUNX2.

85 he IHC examination of human CCA specimen for VDR revealed that higher VDR expression was linked with

86 in common in both groups contained frequent VDR sites that likely regulated their expression.

87 Mesenteric lymph node cultures from VDR KO and B-VDR KO mice secreted higher IgE ex vivo tha

88 Furthermore, VDR 4-1 therapy significantly suppressed cardiac hypertr

89 ith 25(OH)D were found for SNPs in genes GC, VDR, CYP2R1, and CYP27B1.

90 ter activity, regulate VDR downstream genes (VDR, CYP24A1, TRPV6 and CYP27B1), and inhibit the produc

91 ts in 7 vitamin D and calcium pathway genes (VDR, GC, DHCR7, CYP2R1, CYP27B1, CYP24A1, and CASR) modi

92 ies suggest they may act on this non-genomic VDR site.

93 vitamin D analogues 12 and 26 retained good VDR binding ability.

94 an CCA specimen for VDR revealed that higher VDR expression was linked with better prognosis.

95 after the first noncoding exon of the human VDR gene.

96 We also identified VDR-binding sites across the Vdr gene locus in kidney an

97 In VDR knockout mouse epithelial cells (KO), 1,25(OH)2D3 in

98 In VDR wildtype mouse corneal epithelial cells (WT), 1,25(O

99 ls led to significant decreased Claudin-2 in VDR(-/-) and VDR(DeltaIEC) mice.

100 The carrier state of A allele in VDR rs2228570 and CYP2R1 rs10741657 genes were independe

101 PPARgamma suppression underlies alopecia in VDR(-/-) mice.

102 ted PPARgamma suppression causes alopecia in VDR-null mice.

103 y observed but the potential for a change in VDR interaction at the genome as well.

104 quence variant (c.2 T > C; p.1Met?) found in VDR is an initiation coding change and was detected in c

105 The increase in IgE in VDR KO mice was 2-fold greater than in the B-VDR KO mice

106 ficiency normalized PPARgamma mRNA levels in VDR(-/-) keratinocytes and restored anagen responsivenes

107 sion on IL-10 secreting B cells was lower in VDR KO mice.

108 Nine polymorphisms in VDR, CYP24A, CYP27B1, GC, and RXRA were analyzed as effe

109 entially expressed genes are up-regulated in VDR(-/-) KSCs; thus, the VDR is a transcriptional suppre

110 PPARgamma interacts with these sequences in VDR(-/-) but not WT keratinocytes.

111 of the intervention were modified by SNPs in VDR and CYP27B1.

112 r interactions between allelic variations in VDR and RXRG genes on metabolic outcomes; however, furth

113 nd restored anagen responsiveness in vivo in VDR(-/-) mice, resulting in hair regrowth.

114 mation, demonstrating how such inhibition is VDR-dependent.

115 estinal epithelial VDR conditional knockout (VDR(DeltaIEC)) mice, and cultured human intestinal epith

116 siRNA-mediated VDR knock-down reversed the inhibitory effect of calcitr

117 Six of those genes (STAT4, JAK2, MX1, VDR, DDX58, and EIF2AK2) also showed significant associa

118 Notably, VDR occupancy of the PPARgamma regulatory region preclud

119 mors with high expression of stromal nuclear VDR [>/=30 ng/mL vs. <30 ng/mL RR (95% CI): VDR >/= medi

120 VDR-null (VDR(-/-)) mice exhibit lack of postmorphogenic hair cycl

121 ,25-D3 or calcitriol), a naturally occurring VDR agonist, VDR 4-1 therapy even at high doses did not

122 Absence of VDR decreased Claudin-2 expression by abolishing VDR/pro

123 Thus, absence of VDR-mediated PPARgamma suppression underlies alopecia in

124 uence tailor the transcriptional activity of VDR toward specific target genes.The vitamin D receptor/

125 In contrast, AF2 of VDR within VDRM:BGLAP bound heterodimer is more vulnerab

126 bility shift assays showed direct binding of VDR to enhancer regions of SHP.

127 ipt and protein expression concentrations of VDR, E-cadherin, and occludin as well as decreased prote

128 Depletion of VDR-binding sites in OBs, due in part to reduced VDR exp

129 To localize effects of VDR deficiency to hematopoietic cells and to avoid the m

130 iadipogenic and the antimicrobial effects of VDR, indicating a link between VDR and PPARgamma signali

131 ons correlate with the mucosal expression of VDR as well as epithelial junction proteins and inversel

132 Increased expression of VDR by progesterone allows highly sensitive regulation o

133 We also show expression of VDR in OLG lineage cells in multiple sclerosis.

134 Genotyping of VDR polymorphisms (FokI, BsmI, ApaI, and TaqI) was perfo

135 The impact of VDR, RUNX2, and C/EBPbeta on osteoblast differentiation

136 KBR3 expressed significantly lower levels of VDR but higher levels of CD44 expression.

137 ith risk of tumors expressing high levels of VDR.

138 ,25(OH)2D3], the endogenous active ligand of VDR, resulted in higher brain P-glycoprotein (P-gp) and

139 These results indicate that loss of VDR restricts the adaptation to cholestasis and diminish

140 ression, was the likely cause of the loss of VDR-target gene interaction.

141 known ligands and downstream metabolites of VDR.

142 e Vdr and hint at the differential nature of VDR binding activity at the Vdr gene in different primar

143 a novel mechanism of negative regulation of VDR-mediated transcription.

144 tic factors contribute to down regulation of VDR.

145 enhanced expression of SNAIL, a repressor of VDR.

146 However, a number of additional sites of VDR binding unique to either kidney or intestine were pr

147 hibitor lacking the secosteroid structure of VDR ligand antagonists.

148 suppressed transcription and translation of VDR.

149 for association between survival and 25-OHD, VDR genotype/haplotype, and after applying a VDR genotyp

150 tamin D, there is a dearth of information on VDR gene polymorphisms and breast cancer among African-A

151 nt exposure >/= 1 hr/day of sunlight and one VDR haplotype was less than expected given negative HRs

152 haplotypes increased eczema risk whereas one VDR haplotype lowered eczema risk.

153 ell regulation independent of 1,25(OH)2D3 or VDR.

154 Placental VDR expression was assessed via Western blot and validat

155 Placental VDR expression was inversely associated with neonatal 25

156 Placental VDR was a positive predictor of fetal femur length Z sco

157 The association between placental VDR and fetal long bone length may indicate a role for V

158 elation to fetal long bone length, placental VDR, serum 25-hydroxyvitamin D [25(OH)D], 1,25-dihydroxy

159 The fetus may regulate placental VDR expression given the significant associations with n

160 s using known risk factors and, potentially, VDR SNPs.

161 and fibrosis through its ability to promote VDR signaling in HSCs, whose activation supports HCC.

162 nce suggests that vitamin D and its receptor VDR may regulate intestinal barrier function.

163 tro and mice without the vitamin D receptor (VDR knockout [KO]) have high serum IgE.

164 ets were associated with vitamin D receptor (VDR) (rs2228570, P = 0.002, q = 0.04) and MMP3 (rs520540

165 of binding sites for the vitamin D receptor (VDR) across the proximal intestine in vitamin D-sufficie

166 Vitamin D receptor (VDR) activation in HSCs inhibits liver inflammation and

167 re, we document that the vitamin D receptor (VDR) acts as a master transcriptional regulator of autop

168 ll types, while use of a vitamin D receptor (VDR) agonist (EB1089) and antagonist (23S,25S)-DLAM-2P c

169 rough down regulation of vitamin D receptor (VDR) and activation of renin angiotensin system; however

170 d an association between vitamin D receptor (VDR) and lipid metabolism in human tuberculosis and infe

171 east tumor expression of vitamin D receptor (VDR) and retinoid X receptor-alpha (RXR) has not been in

172 ion between the inactive vitamin D receptor (VDR) and Stat1, which was released upon stimulation with

173 ssed localization of the vitamin D receptor (VDR) at sites of action on a genome-scale using ChIP seq

174 tamin D treatment led to vitamin D receptor (VDR) binding in the promoter region of OX40L and signifi

175 marked downregulation of vitamin D receptor (VDR) during OIS, and a role for the vitamin D/VDR axis r

176 Recently, we found that vitamin D receptor (VDR) enhanced Claudin-2 expression in colon and that bil

177 eterminants of placental vitamin D receptor (VDR) expression and placental calcium (Ca) transfer amon

178 The vitamin D receptor (VDR) FokI AA genotype and retinoid X receptor (RXR) rs78

179 Polymorphisms of the vitamin D receptor (VDR) gene have been implicated in susceptibility to infe

180 vel and variation at the vitamin D receptor (VDR) gene locus.

181 and its interaction with vitamin D receptor (VDR) gene variants on breast cancer risk.

182 emonstrate a role of the vitamin D receptor (VDR) in reducing cerebral soluble and insoluble amyloid-

183 terone is a novel inducer of vit.D receptor (VDR) in T cells and makes T cells highly sensitive to ca

184 Here, we reveal that the vitamin D receptor (VDR) is expressed in stroma from human pancreatic tumors

185 The vitamin D receptor (VDR) is the single known regulatory mediator of hormonal

186 Vitamin D receptor (VDR) knockdown partly abolished MART-10-induced inhibiti

187 Here, we show that vitamin D receptor (VDR) ligands inhibit HSC activation by TGFbeta1 and abro

188 Vitamin D receptor (VDR) mutations in humans and mice cause alopecia.

189 about the effects of the vitamin D receptor (VDR) on hepatic activity of human cholesterol 7alpha-hyd

190 ke and activation of the vitamin D receptor (VDR) pathway in colon cancer cells that expressed one of

191 the association between vitamin D receptor (VDR) polymorphisms and genetic susceptibility to compone

192 1,25D3 alters vitamin D receptor (VDR) recruitment to the Cyp11a1 promoter in vitro and in

193 The role of the vitamin D receptor (VDR) was also examined.

194 Vitamin D receptor (VDR) was significantly down-regulated in mammospheres, a

195 (CYP2R1)(rs10741657AG), vitamin D receptor (VDR)(rs2228570AG, rs1544410CT), oligoadenylate synthetas

196 It is the ligand of the vitamin D receptor (VDR), a nuclear receptor with transactivating capacity.

197 The vitamin D receptor (VDR), an endocrine nuclear receptor for 1alpha,25-dihydr

198 pounds that activate the vitamin D receptor (VDR), but are devoid of hypercalcemia.

199 ession concentrations of vitamin D receptor (VDR), E-cadherin, zonula occluden 1 (ZO-1), occludin, cl

200 erphosphorylation of the vitamin D receptor (VDR), enabling an interaction between VDR and the coacti

201 h mast cells express the vitamin D receptor (VDR), it is not clear to what extent 1alpha,25-dihydroxy

202 are mediated through the vitamin D receptor (VDR), which heterodimerizes with retinoid X receptor, ga

203 ranscription factor, the vitamin D receptor (VDR), whose activating ligand vitamin D has been propose

204 2D3) are mediated by the vitamin D receptor (VDR), whose expression in bone cells is regulated positi

205 H)2D3 interacts with the vitamin D receptor (VDR), with similar potency to its native ligand, 1alpha,

206 Absence of vitamin D receptor (VDR)-mediated PPARgamma suppression causes alopecia in V

207 of SWI/SNF and PRMTs in vitamin D receptor (VDR)-mediated transcription.

208 Both VDREs bound the vitamin D receptor (VDR)-retinoid X receptor (RXR) complex and drove reporte

209 nd OLGs, one of which is vitamin D receptor (VDR).

210 ta (C/EBPbeta), OSX, and vitamin D receptor (VDR).

211 mechanisms involving the vitamin D receptor (VDR).

212 liganded heterodimers of vitamin D receptor (VDR)/RXR-alpha and retinoic acid receptor-gamma (RAR-gam

213 r immune cell expression of the VD receptor (VDR) impacts costimulatory blockade induced cardiac allo

214 helial cells (LECs) expressed VitD Receptor (VDR), both on mRNA and protein levels.

215 ficantly associated with bile acid receptors VDR and TGR5 expression.

216 ession in colon and that bile salt receptors VDR and Takeda G-protein coupled receptor5 (TGR5) were h

217 Vitamin D receptors (VDRs) are found within multiple tissues, including the b

218 o genetic variations in vitamin D receptors (VDRs).

219 binding sites in OBs, due in part to reduced VDR expression, was the likely cause of the loss of VDR-

220 , stimulate VDRE-reporter activity, regulate VDR downstream genes (VDR, CYP24A1, TRPV6 and CYP27B1),

221 AC) individually could optimally up regulate VDR in HIV milieu.

222 or complex in HIV milieu that down regulates VDR expression.

223 Vitamin D related (VDR rs2228570 and CYP2R1 rs10741657) and IL28B rs1297986

224 Replicated VDR-BVs associated with these disorders could represent

225 In this stringent test, these replicated VDR-BVs were significantly (q < 0.1) and substantially (

226 en combined were successful in de-repressing VDR expression.

227 The residual VDR cistrome was composed of 4617 sites, which was incre

228 SHP) promoter and deletion analyses revealed VDR-dependent inhibition of SHP, and mobility shift assa

229 Using an RXR-VDR mammalian two-hybrid (M2H) biologic assay system, we

230 al and knockdown approaches we show that RXR-VDR signaling induces OPC differentiation and that VDR a

231 ur findings are consistent with altered RXR::VDR binding contributing to immunity-related diseases.

232 e approach's validity is underscored by RXR::VDR motif sequence being predictive of binding strength

233 VDR-BVs are enriched in consensus RXR::VDR binding motifs, yet most fell outside of these motif

234 this adverse effect is to develop selective VDR modulators (VDRMs) that differentially activate BGLA

235 ted with early AMD, 4 SNPs (RXRA) and 1 SNP (VDR) were associated with nvAMD, and 1 SNP (RXRA), 2 SNP

236 ciated with nvAMD, and 1 SNP (RXRA), 2 SNPs (VDR), and 1 SNP (CYP2R1) were associated with late AMD.

237 Two SNPs (VDR) were associated with early AMD, 4 SNPs (RXRA) and 1

238 ell-specific VDR (T-VDR) KO, B cell-specific VDR (B-VDR) KO, and vitamin D deficient mice were used t

239 Whole-body VDR KO, T cell-specific VDR (T-VDR) KO, B cell-specific VDR (B-VDR) KO, and vita

240 ect WT cell proliferation, but did stimulate VDR KO cell proliferation.

241 d divergent roles for central nervous system VDR signaling.

242 avoid the metabolic consequences of systemic VDR deficiency, we produced bone marrow (BM)-chimeric mi

243 Whole-body VDR KO, T cell-specific VDR (T-VDR) KO, B cell-specific VDR (B-VDR) KO, and vitamin D d

244 B-VDR KO mice developed hyper-IgE, whereas T-VDR KO mice did not.

245 gnaling induces OPC differentiation and that VDR agonist vitamin D enhances OPC differentiation.

246 antagonist (23S,25S)-DLAM-2P confirmed that VDR pathway activation was required for this response.

247 is idea was confirmed through discovery that VDR cistromes in POBs and OBs were also strikingly diffe

248 We found that VDR colocalized with and activated key appetite-regulati

249 We show that VDR acts as a master transcriptional regulator of PSCs t

250 Our data showed that VDR-enhances Claudin-2 promoter activity in a Cdx1 bindi

251 r than in the B-VDR KO mice, suggesting that VDR deficiency in non-B cells contributes to hyper-IgE i

252 The VDR directly and indirectly regulates IgE production in

253 indings point to a role of vitamin D and the VDR in modulating autophagy and cell death in both the n

254 18, respectively), and GAGC haplotype at the VDR locus for all-cause mortality (P = .008).

255 esence of the SNAIL repressor complex at the VDR promoter.

256 here was an increased CpG methylation at the VDR promoter.

257 amine for potential interactions between the VDR and RXRG gene polymorphisms in the 1958BC.

258 kidney tissue, and none were occupied by the VDR in the intestine, consistent with weak or absent reg

259 Furthermore, the VDR axis also modulates non-Smad signaling by activating

260 Our findings identify the VDR as a novel suppressor of IFN-alpha-induced signaling

261 ons between the tagging polymorphisms in the VDR (22 tag SNPs) and RXRG (23 tag SNPs) genes on metabo

262 Polymorphisms in the VDR gene (ApaI, BsmI, and TaqI) were assessed to determi

263 To examine whether the polymorphisms in the VDR gene are associated with the development of NMSC and

264 ingle-nucleotide polymorphisms (SNPs) in the VDR, resulting in contradictory findings as to whether t

265 taxa at multiple genetic loci, including the VDR gene (encoding vitamin D receptor).

266 mad signaling by the specific binding of the VDR along with its heterodimeric partner RXR to the nega

267 Activation of the VDR by vitamin D induces autophagy and an autophagic tra

268 ingle nucleotide polymorphisms (SNPs) of the VDR gene were genotyped.

269 Activation of the VDR represses hepatic SHP to increase levels of mouse an

270 ne with these observations, silencing of the VDR resulted in an enhanced hepatocellular response to I

271 ts ability to stimulate translocation of the VDR to the nucleus, stimulate VDRE-reporter activity, re

272 Sequencing analysis of the VDR, CYP24A1, CYP27B1 and CYP2R1 detected twelve nucleot

273 ealed the independent predictor value of the VDR-FokI polymorphism for DFS.

274 ludes action through the genomic site of the VDR.

275 buried, is anchored to a site located on the VDR surface.

276 The composite data suggest that the VDR is an important therapeutic target in the prevention

277 Through the VDR, vitamin D is an environmental factor that helps to

278 are up-regulated in VDR(-/-) KSCs; thus, the VDR is a transcriptional suppressor in WT KSCs.

279 r, suggested that factors in addition to the VDR might also be involved.

280 he 20S-OH moiety and the 25-OH moiety to the VDR, which may explain some differences in their biologi

281 particularly in the hippocampus in which the VDR is abundant and P-gp induction is greatest after 1,2

282 This contrasts with the VDR and PPARgamma co-occupancy observed on PGC1beta and

283 y, low HDL and T2DM were associated with the VDR gene.

284 ancreatic tumors and that treatment with the VDR ligand calcipotriol markedly reduced markers of infl

285 ow that VitD is anti-lymphangiogenic through VDR-dependent anti-proliferative and pro-apoptotic mecha

286 upplementation in T2DM patients according to VDR polymorphisms.

287 In conclusion, we have identified a unique VDR agonist compound with beneficial effects in mouse mo

288 ensitivity, an effect that is dependent upon VDR within the paraventricular nucleus of the hypothalam

289 In vivo, VDR deletion in intestinal epithelial cells led to signi

290 et gene of 1,25(OH)2D3; its upregulation was VDR-dependent and a functional VDRE in the promoter was

291 This study examines whether VDR gene polymorphisms are associated with breast cancer

292 (CP) in a Thai population is associated with VDR polymorphisms.

293 recancerous lesions and its association with VDR and TGR5 expression.

294 ctions with the A-pocket in conjunction with VDR translocation studies suggest they may act on this n

295 ding protein (C/EBP) beta and cooperate with VDR and C/EBPbeta in regulating Cyp24a1 transcription.

296 s its nuclear localization, interaction with VDR, intra-nuclear trafficking, and binding to chromatin

297 p62 directly interacts with VDR and RXR promoting their heterodimerization, which is

298 t levels were restored on replenishment with VDR ligands.

299 nst background sets of variants lying within VDR-binding regions that had been matched in allele freq

300 The crystal structure of the zebrafish VDR ligand binding domain in complex with LCA and the SR