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1 CYP27B1 expression was not affected by vitamin D(3) and
2 ochrome P450 family 27 subfamily B member 1 (CYP27B1) and CYP24A1 function to maintain physiological
3 ochrome P450 family 27 subfamily B member 1 (CYP27B1), whose gene is regulated by parathyroid hormone
4 etabolites among pregnant women [including a CYP27B1-associated increase in 1,25(OH)2D3] and the evid
6 sion of cytochrome P450 enzyme (CYP)27A1 and CYP27B1, however, having only slight effect on CYP24.
7 In HCEC, 24,25(OH)2D3 increased CYP24A1 and CYP27B1 mRNA and protein expression, and stimulated cell
8 n the other hand, increased both CYP24A1 and CYP27B1 protein expression in WT and VDR KO cells, and s
10 ndrial cytochrome P450s (CYP24A, CYP27A, and CYP27B1) has been described that catalyze the formation
13 rted association between type 1 diabetes and CYP27B1 (P = 1.4 x 10(-4)), we obtained consistent evide
14 the vitamin D-binding protein gene (Gc) and CYP27B1 and CYP24A1, which code for enzymes that, respec
15 DR downstream genes (VDR, CYP24A1, TRPV6 and CYP27B1), and inhibit the production of inflammatory mar
19 ans, there are positive correlations between CYP27B1 and SLC23A1 expression levels in kidney (r = 0.7
22 ihydroxyvitamin D (1,25D), is synthesized by CYP27B1 from 25-dihydroxyvitamin D (25D) and is inactiva
26 Sequencing analysis of the VDR, CYP24A1, CYP27B1 and CYP2R1 detected twelve nucleotide changes in
27 iated steps of vitamin D activation (CYP2R1, CYP27B1) and inactivation (CYP24A1, CYP3A4) and the newe
28 ve vitamin D-related genes (CYP27A1, CYP2R1, CYP27B1, GC and VDR) were genotyped in 1442 Chinese chil
29 lcium pathway genes (VDR, GC, DHCR7, CYP2R1, CYP27B1, CYP24A1, and CASR) modify the effects of vitami
30 D receptor (VDR), and the P450 cytochromes, CYP27B1 and CYP24A1; however, they have yet to be invest
33 5-hydroxyvitamin D-1alpha-hydroxylase (i.e., CYP27B1), leading to enhanced bioconversion of 25-hydrox
34 tion, and on the vitamin D activating enzyme CYP27B1 (produces 1,25(OH)2D3) and inactivating enzyme C
35 itD) receptor and the VitD-activating enzyme CYP27B1, permitting T cells to both activate and respond
36 form (calcitriol) by the hydroxylase enzyme CYP27B1 In multiple sclerosis lesions, the tyrosine kina
41 olon cancer cells that expressed one of five CYP27B1 single-nucleotide polymorphisms (SNP) or four CY
42 red with the wild-type control, four of five CYP27B1 SNPs reduced enzymatic activity, whereas one (V1
43 ence of association with type 1 diabetes for CYP27B1 -1260 and +2838 polymorphisms, which are in perf
47 has recently been reported that heterozygous CYP27B1 mutations are associated with increased MS susce
49 g 25-hydroxyvitamin D(3) 1alpha-hydroxylase (CYP27B1(-/-)), and having no circulating 1,25(OH)(2)D(3)
51 amin D-activating enzyme 1alpha-hydroxylase (CYP27B1) and vitamin D receptor (VDR) support anti-infla
52 of CYP2R1 with vitamin D 1alpha-hydroxylase (CYP27B1) elicited additive activation of vitamin D3, whe
53 covery of the extrarenal 1alpha-hydroxylase (CYP27B1) in various vitamin D target tissues around the
55 of 25-hydroxyvitamin D3-1alpha-hydroxylase (CYP27B1) mRNA was markedly increased in renal proximal c
56 yme 25-hydroxyvitamin D3-1alpha-hydroxylase (CYP27B1), which can be expressed by activated immune cel
57 -regulated expression of 1alpha-hydroxylase (CYP27B1, 1alphaOHase), the enzyme that converts 25-hydro
58 and 25-hydroxyvitamin D 1alpha-hydroxylase (CYP27B1: rs4646536) (adjusted hazard ratio >/= 1.47; P f
60 m genes CYP2R1 and CYP27A1 (25-hydroxylase), CYP27B1 (1-alpha-hydroxylase), and vitamin D receptor (V
61 would describe presence of VDR, hydroxylases CYP27B1 and CYP24A1, and RORalpha and RORgamma in the hu
65 ke receptor 2/1 heterodimer (TLR2/1)-induced CYP27B1 and IL1B expression as well as indirectly upregu
66 Blocking the vitamin D receptor, inhibiting CYP27B1, or limiting 25D3 availability prevented TGF-bet
73 ntly, CT greatly increased the expression of CYP27B1 mRNA in the kidney of normocalcemic sham-TPTX ra
75 tion of PTH did not induce the expression of CYP27B1 mRNA in the kidney of vitamin D-replete sham-TPT
78 was explained by findings that the levels of CYP27B1, which converts 25OH vitamin D3 (25D3) to active
86 d calcitonin (CT) on the expression of renal CYP27B1 mRNA was investigated in normocalcemic sham-oper
87 c state, the mechanism to regulate the renal CYP27B1 gene could be different, since plasma levels of
88 and inactivating hydroxylases, respectively, CYP27B1 and CYP24A1, and the retinoic acid-related orpha
91 aim was to study the association between the CYP27B1 and CYP24A1 gene polymorphisms and type 1 diabet
92 he enzyme 1 alpha-hydroxylase encoded by the CYP27B1 gene and is inactivated by 24-hydroxylase encode
93 sclerosis and the rare mutant alleles of the CYP27B1 gene responsible for autosomal recessive vitamin
95 n convert 25OHD3 to 1alpha,25(OH)2D3 through CYP27B1 activity and that both of these vitamin D3 metab
96 CYP24A1, having selectivity with respect to CYP27B1 comparable with or greater than that of the stan
97 against colorectal neoplasms, and CaR, VDR, CYP27B1, and CYP24A1 as modifiable, preneoplastic risk b
99 We further analyzed the expression of VDR, CYP27B1, CYP24A1, and ROR in relation to melanin levels,
100 elop chemically induced skin tumors, whereas CYP27B1(-/-) and wild-type mice do not, indicating that
101 CD14, or TLR2 in human keratinocytes, while CYP27B1-deficient mice failed to increase CD14 expressio