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1 etabolites among pregnant women [including a CYP27B1-associated increase in 1,25(OH)2D3] and the evid
3 sion of cytochrome P450 enzyme (CYP)27A1 and CYP27B1, however, having only slight effect on CYP24.
4 In HCEC, 24,25(OH)2D3 increased CYP24A1 and CYP27B1 mRNA and protein expression, and stimulated cell
5 n the other hand, increased both CYP24A1 and CYP27B1 protein expression in WT and VDR KO cells, and s
7 ndrial cytochrome P450s (CYP24A, CYP27A, and CYP27B1) has been described that catalyze the formation
10 rted association between type 1 diabetes and CYP27B1 (P = 1.4 x 10(-4)), we obtained consistent evide
11 the vitamin D-binding protein gene (Gc) and CYP27B1 and CYP24A1, which code for enzymes that, respec
12 DR downstream genes (VDR, CYP24A1, TRPV6 and CYP27B1), and inhibit the production of inflammatory mar
20 Sequencing analysis of the VDR, CYP24A1, CYP27B1 and CYP2R1 detected twelve nucleotide changes in
21 iated steps of vitamin D activation (CYP2R1, CYP27B1) and inactivation (CYP24A1, CYP3A4) and the newe
22 ve vitamin D-related genes (CYP27A1, CYP2R1, CYP27B1, GC and VDR) were genotyped in 1442 Chinese chil
23 lcium pathway genes (VDR, GC, DHCR7, CYP2R1, CYP27B1, CYP24A1, and CASR) modify the effects of vitami
24 D receptor (VDR), and the P450 cytochromes, CYP27B1 and CYP24A1; however, they have yet to be invest
26 5-hydroxyvitamin D-1alpha-hydroxylase (i.e., CYP27B1), leading to enhanced bioconversion of 25-hydrox
27 tion, and on the vitamin D activating enzyme CYP27B1 (produces 1,25(OH)2D3) and inactivating enzyme C
32 olon cancer cells that expressed one of five CYP27B1 single-nucleotide polymorphisms (SNP) or four CY
33 red with the wild-type control, four of five CYP27B1 SNPs reduced enzymatic activity, whereas one (V1
34 ence of association with type 1 diabetes for CYP27B1 -1260 and +2838 polymorphisms, which are in perf
37 has recently been reported that heterozygous CYP27B1 mutations are associated with increased MS susce
39 g 25-hydroxyvitamin D(3) 1alpha-hydroxylase (CYP27B1(-/-)), and having no circulating 1,25(OH)(2)D(3)
41 amin D-activating enzyme 1alpha-hydroxylase (CYP27B1) and vitamin D receptor (VDR) support anti-infla
42 of CYP2R1 with vitamin D 1alpha-hydroxylase (CYP27B1) elicited additive activation of vitamin D3, whe
43 covery of the extrarenal 1alpha-hydroxylase (CYP27B1) in various vitamin D target tissues around the
45 of 25-hydroxyvitamin D3-1alpha-hydroxylase (CYP27B1) mRNA was markedly increased in renal proximal c
46 yme 25-hydroxyvitamin D3-1alpha-hydroxylase (CYP27B1), which can be expressed by activated immune cel
47 -regulated expression of 1alpha-hydroxylase (CYP27B1, 1alphaOHase), the enzyme that converts 25-hydro
48 and 25-hydroxyvitamin D 1alpha-hydroxylase (CYP27B1: rs4646536) (adjusted hazard ratio >/= 1.47; P f
53 ke receptor 2/1 heterodimer (TLR2/1)-induced CYP27B1 and IL1B expression as well as indirectly upregu
54 Blocking the vitamin D receptor, inhibiting CYP27B1, or limiting 25D3 availability prevented TGF-bet
60 ntly, CT greatly increased the expression of CYP27B1 mRNA in the kidney of normocalcemic sham-TPTX ra
62 tion of PTH did not induce the expression of CYP27B1 mRNA in the kidney of vitamin D-replete sham-TPT
64 was explained by findings that the levels of CYP27B1, which converts 25OH vitamin D3 (25D3) to active
72 d calcitonin (CT) on the expression of renal CYP27B1 mRNA was investigated in normocalcemic sham-oper
73 c state, the mechanism to regulate the renal CYP27B1 gene could be different, since plasma levels of
76 aim was to study the association between the CYP27B1 and CYP24A1 gene polymorphisms and type 1 diabet
77 he enzyme 1 alpha-hydroxylase encoded by the CYP27B1 gene and is inactivated by 24-hydroxylase encode
78 sclerosis and the rare mutant alleles of the CYP27B1 gene responsible for autosomal recessive vitamin
80 n convert 25OHD3 to 1alpha,25(OH)2D3 through CYP27B1 activity and that both of these vitamin D3 metab
81 CYP24A1, having selectivity with respect to CYP27B1 comparable with or greater than that of the stan
82 against colorectal neoplasms, and CaR, VDR, CYP27B1, and CYP24A1 as modifiable, preneoplastic risk b
84 elop chemically induced skin tumors, whereas CYP27B1(-/-) and wild-type mice do not, indicating that
85 CD14, or TLR2 in human keratinocytes, while CYP27B1-deficient mice failed to increase CD14 expressio
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