ライフサイエンスコーパス: VDR

1 VDR 4-1 also effectively suppressed secondary hyperparat

2 VDR activation exerts anti-inflammatory effects in immun

3 VDR and RXR expression were assessed by immunohistochemi

4 VDR associated with PU.1 in Th9 cells.

5 VDR expression could potentially be used as a biomarker

6 VDR expression is induced in hepatic macrophages by ER s

7 VDR expression was independently protective for melanoma

8 VDR modifies gene expression by binding DNA as a heterod

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

10 VDR signaling in macrophages regulates a shift between p

11 VDR(-/-) and VDD diabetic mice (diabetic for 8 and 20 we

12 VDR(-/-) and VDD diabetic mice also showed significantly

13 VDR(DeltaPC) mice also showed high susceptibility to sma

14 VDR(DeltaPC) mice had significantly higher inflammation

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

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

17 VDR-occupied sites were present in both the kidney and N

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

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

20 (95% CI): VDR >/= median = 0.67 (0.48-0.93); VDR < median = 0.98 (0.72-1.35), P heterogeneity = 0.12]

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

22 shortened survival in primary melanoma in a VDR-dependent manner.

23 B2-dependent gene upregulation, suggesting a VDR-independent anti-inflammatory effect of paricalcitol

24 Additionally, VDR and CYP27B1 expression levels were measured.

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

26 HFD was more pronounced in female mice after VDR deletion.

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

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

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

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

31 scue experiments, we confirmed vitamin D and VDR inhibited LPS- or activated CD4(+) T cell-induced mi

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

33 Co-housing of VDR(DeltaPC) and VDR(lox) mice made the VDR(DeltaPC) less vulnerable to d

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

35 of 25-hydroxylase, 1-alpha-hydroxylase, and VDR, and hypomethylation of CYP24A1 was observed in HFD-

36 We used in vivo VDR(lox) and VDR(DeltaIEC) mice and ex vivo organoids generated from

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

38 ced in hepatic macrophages by ER stress, and VDR plays a dual regulatory role in macrophages by prote

39 llus and crypt were found to express Vdr and VDR target genes.

40 4A1 and CYP27B1 protein expression in WT and VDR KO cells, and stimulated cell proliferation in both

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

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

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

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

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

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

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

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

49 /-) mice, and an inverse correlation between VDR and miR-802 was found in human biopsy specimens of O

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

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

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

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

54 e repression of fibrosis and inflammation by VDR agonists.

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

56 ential gut-liver-microbiome axis mediated by VDR that might trigger downstream metabolic disorders.

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

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

59 g had organ-restricted effects, with cardiac VDR activation causing cardiomegaly.

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

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

62 Conditional VDR deletion severely changed metabolites specifically p

63 through the TLR2-dependent p38-MAPK-CYP27B1-VDR signaling pathway.

64 e of a causal relationship between vitamin D-VDR signaling and melanoma survival, which should be exp

65 riptomes to understand the role of vitamin D-VDR signaling and replicated the findings in The Cancer

66 In summary, vitamin D-VDR signaling contributes to controlling pro-proliferati

67 ation studies showed that elevated vitamin D-VDR signaling inhibited Wnt/beta-catenin signaling genes

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

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

70 In sum, our results show that vitamin D/VDR signaling induces miR-27a/b in oral lichen planus.

71 Vitamin D/VDR signaling suppresses microRNA-802-induced apoptosis

72 ollectively, our data suggest that vitamin D/VDR signaling suppresses oral keratinocyte apoptosis by

73 In addition, vitamin D/VDR signaling was able to suppress miR-802 expression in

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

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

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

77 cantly increased after intestinal epithelial VDR deletion and were further increased by the high-fat

78 In summary, intestinal epithelial VDR regulates autophagy and apoptosis through ATG16L1 an

79 the mechanisms of the intestinal epithelial VDR regulation of autophagy and apoptosis.

80 -skeletal example of a tissue that expresses VDR that not only makes vitamin D but also can metaboliz

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

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

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

84 sion was enhanced in oral keratinocytes from VDR(-/-) mice, and an inverse correlation between VDR an

85 endotoxin levels were high in the serum from VDR(DeltaIEC) mice and made mice susceptible to colitis.

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

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

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

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

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

91 the following order: RARalpha > PPARgamma > VDR.

92 presentation of transcription factors HIF1A, VDR, and CLOCK, among others, and of GO term pathways re

93 High VDR-expressing tumors had downregulation of proliferativ

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

95 In VDR knockout mice with renal injury, paricalcitol preven

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

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

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

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

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

101 s of Beclin-1 and lysozyme were decreased in VDR(DeltaIEC) organoids.

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

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

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

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

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

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

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

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

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

111 Standard PgLPS and Pam3CSK4 increased VDR expression in the presence of vitamin D(3) .

112 (-/-) mice, vitamin D(3) treatment increased VDR and ATG16L1 protein expression levels, which activat

113 We identified the decreased intestinal VDR significantly correlated with reduction of an inflam

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

115 Isolated VDR(DeltaPC) Paneth cells exhibited weakened inhibition

116 the effects of vitamin D receptor knockout (VDR(-/-)) and vitamin D deficiency (VDD) on corneal epit

117 generated Paneth cell-specific VDR knockout (VDR(DeltaPC)) mice to investigate the molecular mechanis

118 tment of co-regulatory complexes by liganded VDR leads to changes in gene expression that result in d

119 Deleterious low VDR levels resulted from promoter methylation and gene d

120 Activation of liver macrophage VDRs by vitamin D ligands ameliorates liver inflammation

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

122 ic inflammation conditions of the DIO model, VDR activation by the vitamin D analog calcipotriol redu

123 Moreover, VDR deficiency promotes hepatic macrophage infiltration

124 Muscle VDR-KD elicited atrophy through a reduction in total pro

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

126 Notably, VDR occupancy of the PPARgamma regulatory region preclud

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

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

129 ,25-D3 or calcitriol), a naturally occurring VDR agonist, VDR 4-1 therapy even at high doses did not

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

131 al metabolites are altered in the absence of VDR.

132 f vitamin D production and in the absence of VDR.

133 dicates that the transcriptional activity of VDR is diminished under inflammatory conditions, which m

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

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

136 ll death in the small intestine and colon of VDR(DeltaIEC) mice.

137 s from mice with tissue-specific deletion of VDR in intestinal epithelial cells or myeloid cells.

138 ary contributor to the beneficial effects of VDR activation.

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

140 Ectopic expression of VDR in Th9 cells attenuated the percentage of IL-9-secre

141 We further analyzed the expression of VDR, CYP27B1, CYP24A1, and ROR in relation to melanin le

142 nsights into the tissue-specific function of VDR in modulating the balance between autophagy and apop

143 Thus, the immunomodulatory functions of VDR in macrophages are critical in hepatic ER stress res

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

145 The mammary gland of VDR KO mice shows a florid phenotype revealing alteratio

146 The growth of VDR(DeltaIEC) organoids was significantly slower with fe

147 Co-housing of VDR(DeltaPC) and VDR(lox) mice made the VDR(DeltaPC) les

148 ing muscle atrophy, we studied the impact of VDR knockdown (KD) on mature skeletal muscle in vivo, an

149 ceptor (VDR) only in the distal intestine of VDR null mice (KO/TG mice) results in the normalization

150 Beclin-1 were decreased in the intestines of VDR(DeltaIEC) mice.

151 However, the involvement of VDR in the development of diabetes, specifically in panc

152 Thus, a lack of VDR in Paneth cells leads to impaired antibacterial acti

153 ith risk of tumors expressing high levels of VDR.

154 ct of diet was more prominent due to loss of VDR as indicated by the differences in metabolites gener

155 known ligands and downstream metabolites of VDR.

156 r published, that would describe presence of VDR, hydroxylases CYP27B1 and CYP24A1, and RORalpha and

157 optimal folding of the C-terminal region of VDR.

158 Here, we aimed to study the role of VDR in beta-cells in the pathophysiology of diabetes.

159 The nearly 150 crystal structures of VDR's ligand-binding domain with various vitamin D compo

160 slower with fewer Paneth cells than that of VDR(+/+) organoids.

161 sights into the tissue-specific functions of VDRs in maintaining Paneth cell alertness to pathogens i

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

163 paricalcitol-treated, vitamin D deficient or VDR knockout mice.

164 Murine melanoma cells overexpressing VDR produced fewer pulmonary metastases than controls in

165 In addition, transgenic mice overexpressing VDR in beta-cells were protected against streptozotocin-

166 SNPs in four genes in the vitamin D pathway (VDR, DBP, CYP27B1, CYP24A1) on PCOS.

167 nonsteroidal mimics provided numerous potent VDR agonists and some antagonists.

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

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

170 hown to act through multiple receptors (PXR, VDR, TGR5 and S1PR2), as well as to have receptor-indepe

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

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

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

174 Here we demonstrate that vitamin D receptor (VDR) activation mitigates hepatic ER stress response, wh

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

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

177 Vitamin D receptor (VDR) antagonists prevent the VDR activation function hel

178 Furthermore, we found vitamin D receptor (VDR) binding sites in the promoters of miR-27a/b genes a

179 Vitamin D receptor (VDR) deficiency in the intestine leads to abnormal Panet

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

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

182 Reduced vitamin D receptor (VDR) expression prompts skeletal muscle atrophy.

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

184 , an association between vitamin D receptor (VDR) gene polymorphisms and diabetes has also been descr

185 in the gene encoding the vitamin D receptor (VDR) have been widely reported to associate with suscept

186 Vitamin D receptor (VDR) is a key genetic factor for shaping the host microb

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

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

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

190 sgenic expression of the vitamin D receptor (VDR) only in the distal intestine of VDR null mice (KO/T

191 e-specific modulation of vitamin D receptor (VDR) signaling had organ-restricted effects, with cardia

192 sive effect of vitamin D/vitamin D receptor (VDR) signaling has been shown in the context of oral lic

193 wed by discussion of the vitamin D receptor (VDR) that mediates the cellular actions of 1,25(OH)(2)D.

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

195 -alpha-hydroxylase), and vitamin D receptor (VDR) were downregulated in the livers of mice fed an HFD

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

197 eptor gamma (PPARgamma), vitamin D receptor (VDR), and retinoic acid receptor alpha (RARalpha).

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

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

200 its actions through the vitamin D receptor (VDR), the expression of which was recently confirmed in

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

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

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

204 ene expression levels of vitamin D receptor (VDR)-regulated genes osteocalcin and osteopontin.

205 rmed C24-DS2 binding the vitamin D receptor (VDR).

206 the transcription factor vitamin D receptor (VDR).

207 AE in mice devoid of the vitamin D receptor (VDR).

208 mechanisms involving the vitamin D receptor (VDR).

209 mucosal immunity via the vitamin D receptor (VDR).

210 tamin D3 signals via the vitamin D receptor (VDR).

211 by interacting with the vitamin D receptor (VDR).

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

213 egulation by the vitamin D nuclear receptor (VDR) could provide an alternative route for brain folate

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 is of the expression of vitamin D receptors (VDR), the activating and inactivating hydroxylases, resp

218 ss the highest level of vitamin D receptors (VDRs) among nonparenchymal cells, whereas VDR expression

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

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

221 Genetically and environmentally regulated VDRs in the Paneth cells may set the threshold for the d

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

223 Replicated VDR-BVs associated with these disorders could represent

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

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

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

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

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

229 ogenes, including c-MYC, CD44, CDKN1B, SLUG, VDR, SMAD3, VEGFA, and XBP1.

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

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

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

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

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

235 We generated Paneth cell-specific VDR knockout (VDR(DeltaPC)) mice to investigate the mole

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

237 al transfection was used to induce sustained VDR-KD in C2C12 cells to analyse myogenic regulation.

238 gether, these results suggest that sustained VDR levels in beta-cells may preserve beta-cell mass and

239 d divergent roles for central nervous system VDR signaling.

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

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

242 We conclude that VDR(-/-) and VDD significantly reduce both corneal epith

243 lic effects of calcipotriol, confirming that VDR activation in liver macrophages is required for the

244 Here we found that VDR activation exhibits strong anti-inflammatory effects

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

246 We found that VDR deficiency induced more apoptotic cells and signific

247 erinsulinemic euglycemic clamp revealed that VDR activation greatly increased the glucose infusion ra

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

249 sal and pathogenic microbiota, the role that VDRs in Paneth cells play in these responses is unknown.

250 The VDR directly and indirectly regulates IgE production in

251 The VDR-PU.1 interaction prevented the accessibility of PU.1

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

253 es of mutations, we were able to dissect the VDR domain involved in the regulation of the Il9 gene.

254 vivo electrotransfer (IVE) to knock down the VDR in hind-limb tibialis anterior (TA) muscle for 10 da

255 ransmission of protective bacterial from the VDR(lox) mice.

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

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

258 th cells were significantly decreased in the VDR(DeltaPC) mice.

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

260 een Beclin-1 and Bcl-2 were increased in the VDR-deficient epithelia from mice.

261 2)D, which are disrupted by mutations in the VDR.

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

263 g of VDR(DeltaPC) and VDR(lox) mice made the VDR(DeltaPC) less vulnerable to dextran sulfate sodium c

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

265 In contrast, loss of the VDR cluster in the C24-DS2-deleted strain did not affect

266 ndicate a fundamental regulatory role of the VDR in the regulation of myogenesis and muscle mass, whe

267 dertaken to define the influence loss of the VDR on muscle fibre composition, protein synthesis, anab

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

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

270 ludes action through the genomic site of the VDR.

271 rived from new structural information on the VDR protein.

272 min D receptor (VDR) antagonists prevent the VDR activation function helix 12 from folding into its a

273 se results highlight the autonomous role the VDR has within skeletal muscle mass regulation.

274 Targeting the VDR affects multiple downstream events within Paneth cel

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

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

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

278 that pretreatment of Folr1 KO mice with the VDR activating ligand, calcitriol (1,25-dihydroxyvitamin

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

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

281 upplementation in T2DM patients according to VDR polymorphisms.

282 In response to VDR-knockdown mitochondrial function and related gene-se

283 High tumor VDR expression was associated with upregulation of pathw

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

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

286 In vitro VDR knockdown induces myogenic dysregulation occurring t

287 Finally, in vitro VDR-knockdown impaired myogenesis (cell cycling, differe

288 We used in vivo VDR(lox) and VDR(DeltaIEC) mice and ex vivo organoids ge

289 s (VDRs) among nonparenchymal cells, whereas VDR expression is very low in hepatocytes.

290 esponse of injured zebrafish hearts, whereas VDR blockade inhibited regeneration.

291 itigates hepatic ER stress response, whereas VDR knockout mice undergo persistent UPR activation and

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 noma melanin level inversely correlated with VDR expression.

296 Co-culture with VDR-activated bone marrow-derived macrophages suppresses

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

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

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

300 eport the crystal structure of the zebrafish VDR ligand-binding domain in complex with the ZK168281 a