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1 glutaminase promoter activity in response to 1,25-dihydroxyvitamin D3.
2 M, or IL-1 but not by parathyroid hormone or 1,25-dihydroxyvitamin D3.
3 hormones especially parathyroid hormone and 1,25-dihydroxyvitamin D3.
4 /kg dose for mice proved less effective than 1,25-dihydroxyvitamin D3.
5 at Cdk6 and Cdk2 activities are regulated by 1,25-dihydroxyvitamin D3.
6 e pretreated with the endogenous VDR agonist 1,25-dihydroxyvitamin D3.
7 tory activity of the receptor independent of 1,25-dihydroxyvitamin D3.
8 ed by Salmonella stimulation, independent of 1,25-dihydroxyvitamin D3.
9 of stimulation with the hormonal VDR ligand, 1,25-dihydroxyvitamin D3.
10 200 genes were identified to be regulated by 1,25-dihydroxyvitamin D3.
11 e that is present in most tissues to produce 1,25-dihydroxyvitamin D3.
12 the kidney to its biologically active form, 1,25-dihydroxyvitamin D3.
13 vated extracellular calcium concentration or 1,25-dihydroxyvitamin D3.
14 ablished GADD45 as a primary target gene for 1,25-dihydroxyvitamin D3.
15 C family in keratinocytes and is induced by 1,25-dihydroxyvitamin D3.
16 n markers involucrin and transglutaminase to 1,25-dihydroxyvitamin D3.
17 ects of IL-1, but not parathyroid hormone or 1, 25-dihydroxyvitamin D3.
19 Transcriptional activation in response to 1, 25-dihydroxyvitamin D3 (1,25-(OH)2D3) was virtually e
20 ial amounts of NO on stimulation with LPS or 1, 25-dihydroxyvitamin D3 (1,25-D3) in the absence of ac
21 time-dependent manner above that induced by 1,25 dihydroxyvitamin D3 (1,25 vitamin D3) in cultures o
22 on in human leukemia HL60 cells treated with 1,25 dihydroxyvitamin D3 (1,25D3) at low to moderately h
23 owing that microRNA-498 (miR-498) induced by 1,25-dihydroxyvitamin D3 (1,25(OH)(2)D(3)) decreases the
26 1alpha-hydroxylase, the enzyme required for 1,25-dihydroxyvitamin D3 (1,25(OH)2D3) hormone biosynthe
27 ex, plays a fundamental role in induction by 1,25-dihydroxyvitamin D3 (1,25(OH)2D3) of the transcript
30 itamin D3 (2MD) is a highly potent analog of 1,25-dihydroxyvitamin D3 (1,25(OH)2D3) whose actions are
31 lase (24(OH)ase), a key metabolic enzyme for 1,25-dihydroxyvitamin D3 (1,25(OH)2D3), is up-regulated
32 way against intracellular M. tuberculosis by 1,25-dihydroxyvitamin D3 (1,25(OH)2D3), the active form
34 The ability of the active form of vitamin D, 1,25-dihydroxyvitamin D3 (1,25(OH)2D3), to transcription
35 GF)-23, a bone-derived hormone that inhibits 1,25-dihydroxyvitamin D3 (1,25(OH)2D3; calcitriol) forma
37 tein kinase C (PKC) plays a critical role in 1,25-dihydroxyvitamin D3 (1,25-(OH)2D3) promotion of HL-
43 laboratory has previously demonstrated that 1,25-dihydroxyvitamin D3 (1,25[OH]2D3) rapidly stimulate
45 we show that functional AP-1 is required for 1,25-dihydroxyvitamin D3 (1,25D)-induced monocytic diffe
48 tic differentiation-inducing steroid hormone 1,25-dihydroxyvitamin D3 (1,25D3) and found that growth
50 gical activities and mechanisms of action of 1,25-dihydroxyvitamin D3 (1,25D3) and nine potent 1,25D3
51 In contrast, the active form of vitamin D, 1,25-dihydroxyvitamin D3 (1,25D3), is predominantly immu
53 lated with all-trans retinoic acid (ATRA) or 1,25-dihydroxyvitamin D3 (1,25D3), the biologically acti
54 sms of acquired drug resistance we developed 1,25-dihydroxyvitamin D3 (1,25D3)-resistant sublines of
55 ll (HSNEC) conversion of 25(OH)D3 (25VD3) to 1,25-dihydroxyvitamin D3 (1,25VD3) and, furthermore, tha
58 that AXII gene expression is upregulated by 1,25-dihydroxyvitamin D3 [1, 25-(OH)2D3] and that additi
59 ts in elevated serum phosphate, calcium, and 1,25-dihydroxyvitamin D3 [1,25(OH)(2)D] levels; vascular
61 ne is regulated by extracellular calcium and 1,25-dihydroxyvitamin D3 [1,25(OH)2D3] and GHS rats have
62 ifferentiate normally under the influence of 1,25-dihydroxyvitamin D3 [1,25(OH)2D3] despite the prese
63 single known regulatory mediator of hormonal 1,25-dihydroxyvitamin D3 [1,25(OH)2D3] in higher vertebr
64 nce between bioactivation and degradation of 1,25-dihydroxyvitamin D3 [1,25(OH)2D3] is critical for e
67 estinal Ca hyperabsorption with normal serum 1,25-dihydroxyvitamin D3 [1,25(OH)2D3] levels, elevation
68 le diet (WD) and supplemental calcium and/or 1,25-dihydroxyvitamin D3 [1,25(OH)2D3] on the colorectal
69 e potential functional significance of human 1,25-dihydroxyvitamin D3 [1,25(OH)2D3] receptor (hVDR) p
71 ll stimuli and transcriptional repression by 1,25-dihydroxyvitamin D3 [1,25(OH)2D3] through the vitam
72 In experimental models and clinical trials, 1,25-dihydroxyvitamin D3 [1,25(OH)2D3] was shown to exer
73 itamin D deficiency, and its bioactive form, 1,25-dihydroxyvitamin D3 [1,25(OH)2D3], has been shown t
75 The biologically active form of vitamin D, 1,25-dihydroxyvitamin D3 [1,25(OH)2D3], is able to promo
76 High doses of the active form of vitamin D3, 1,25-dihydroxyvitamin D3 [1,25(OH)2D3], prevent diabetes
77 The receptors for 9-cis retinoic acid and 1,25-dihydroxyvitamin D3 [1,25(OH)2D3], RXR and VDR, res
80 (CYP24A1) with 25(OH)D3, 3-epi-25(OH)D3, and 1,25-dihydroxyvitamin D3 [1,25(OH)2D3]; and 1alpha-hydro
81 ndex over the naturally occurring VDR ligand 1,25-dihydroxyvitamin D3 [1,25-(OH)2D3] in an in vivo pr
83 nal vitamin D receptor (VDR) is required for 1,25-dihydroxyvitamin D3-[1,25(OH)2D3]-induced renal rea
87 nor-1,25-dihydroxyvitamin D2 (200 ng/day) or 1,25-dihydroxyvitamin D3 (50 ng/mouse/day) orally throug
88 retinoid exposure was potently attenuated by 1,25-dihydroxyvitamin D3, a metabolic vitamin derivative
90 To understand the molecular mechanism of 1,25-dihydroxyvitamin D3 action, we profiled the hormone
92 e transient gene expression system augmented 1, 25-dihydroxyvitamin D3-activated transcription, but i
94 Furthermore, CsA causes bone loss, whereas 1,25-dihydroxyvitamin D3 actually increases bone mass.
95 To support this belief, we have found that 1,25-dihydroxyvitamin D3 administration to mice increase
96 m and inositol triphosphate levels following 1,25-dihydroxyvitamin D3 administration were markedly re
99 extremely high serum levels of phosphate and 1,25-dihydroxyvitamin D3, along with abnormal bone miner
101 r patients to benefit from therapy with both 1,25-dihydroxyvitamin D3 and ligands for death receptors
103 aT1 in the intestine is highly responsive to 1,25-dihydroxyvitamin D3 and shows both fast and slow ca
104 Our findings reveal a novel activity of 1,25-dihydroxyvitamin D3 and the VDR in regulation of pr
105 data in the literature support the idea that 1,25-dihydroxyvitamin D3 and the vitamin D receptor (VDR
108 orbol-13-acetate [TPA], gamma interferon, or 1, 25-dihydroxyvitamin D3) and then challenged with HGE.
109 aride (LPS), estradiol, progesterone, and/or 1,25-dihydroxyvitamin D3; and transcriptional activity o
110 tudying the regulation of gene expression by 1,25-dihydroxyvitamin D3, as well as for examining facto
111 ne resorption in organ culture stimulated by 1,25-dihydroxyvitamin D3 at concentrations as low as 75
116 ic acid attenuates the stimulating effect of 1,25-dihydroxyvitamin D3 by decreasing the rate of VDR-R
117 ulture-derived HCV were exposed to bioactive 1,25-dihydroxyvitamin D3 (calcitriol) with or without IF
118 monstrate that the active form of vitamin D, 1,25-dihydroxyvitamin D3 (calcitriol), has a profound in
122 (PTH) significantly (p=0.0172), while serum 1,25-dihydroxyvitamin D3 concentration was not changed b
124 on of the death receptors, pretreatment with 1,25-dihydroxyvitamin D3 decreased apoptosis induced by
125 that endogenous NCoA62/SKIP associated in a 1,25-dihydroxyvitamin D3-dependent manner with VDR targe
127 ver, EVs from osteoclast precursors promoted 1,25-dihydroxyvitamin D3-dependent osteoclast formation
134 DNA or GADD45-null mouse embryo fibroblasts, 1,25-dihydroxyvitamin D3 failed to induce G2/M arrest.
137 how that p21 is transcriptionally induced by 1,25-dihydroxyvitamin D3 in a VDR-dependent, but not p53
138 diator for the tumor-suppressing activity of 1,25-dihydroxyvitamin D3 in human ovarian cancer cells.
142 opriate splicing of transcripts derived from 1,25-dihydroxyvitamin D3-induced expression of a growth
143 important in the signaling pathway mediating 1,25-dihydroxyvitamin-D3-induced keratinocyte differenti
144 in the signal transduction pathway mediating 1,25-dihydroxyvitamin-D3-induced keratinocyte differenti
145 -II and RA 4-hydroxylase, but did not affect 1,25-dihydroxyvitamin D3 induction of the vitamin D rece
146 n A (all-trans retinoic acid) and vitamin D (1,25-dihydroxyvitamin D3) inhibited P. acnes-induced Th1
149 nd normalized serum 25-hydroxyvitamin D3 and 1,25-dihydroxyvitamin D3 levels, as well as mineral and
150 nti-human CD14 Abs blocked the activation of 1,25-dihydroxyvitamin D3-matured human myelomonocytic TH
152 of these two anti-inflammatory cytokines by 1,25-dihydroxyvitamin D3 may be responsible for the abil
154 y important roles in mediating the action of 1,25-dihydroxyvitamin D3 on involucrin expression, but t
155 pproach to overcome the protective effect of 1,25-dihydroxyvitamin D3 on the apoptosis of ovarian can
159 ced osteoclast-like MNC formation induced by 1,25-dihydroxyvitamin D3 or PTH-related protein in mouse
164 Many nuclear receptors, including the human 1,25-dihydroxyvitamin D3 receptor (VDR), bind cooperativ
165 clear hormone receptors, including the human 1,25-dihydroxyvitamin D3 receptor (VDR), bind cooperativ
167 nt studies suggest that growth inhibition by 1,25-dihydroxyvitamin D3 represents an innovative approa
168 esponse element provides specificity for the 1,25-dihydroxyvitamin D3 response lacking at the AP-1 si
169 nhibitor p27 in U937 cells in the absence of 1,25-dihydroxyvitamin D3 results in the cell-surface exp
170 on of Fas relieved the suppressive effect of 1,25-dihydroxyvitamin D3, showing that molecular manipul
171 rived EVs to inhibit osteoclast formation in 1,25-dihydroxyvitamin D3-stimulated marrow cultures.
172 AP-1 site reduced basal activity and blocked 1,25-dihydroxyvitamin D3 stimulation of the involucrin p
173 udy both elements proved to be important for 1,25-dihydroxyvitamin D3 stimulation of the involucrin p
176 the first year of kidney transplantation and 1,25-dihydroxyvitamin D3 supplementation may help reduce
177 ancer cells express vitamin D3 receptors and 1,25-dihydroxyvitamin D3 suppressed growth of these cell
180 These results support the hypothesis that 1, 25-dihydroxyvitamin D3, through interactions with the
181 sity, femurs were collected from nontreated, 1,25-dihydroxyvitamin D3-treated (50 ng/mouse/day), or C
182 were higher in the central nervous system of 1,25-dihydroxyvitamin D3-treated mice compared with cont
183 of cells recoverable from the lymph nodes of 1,25-dihydroxyvitamin D3-treated mice was only 50% that
184 cell line with probes generated from either 1,25-dihydroxyvitamin D3-treated or untreated cells.
190 the multifunctional regulator YY1 represses 1,25-dihydroxyvitamin D3 (vitamin D)-induced transactiva
191 rvival of the transplants brought about with 1,25-dihydroxyvitamin D3 was not accompanied by hypercal
192 n D3 and convert it to the most active form, 1,25-dihydroxyvitamin D3, which regulates keratinocyte p
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