INT160633
From wiki-pain
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Sentences Mentioned In
Key: | Protein | Mutation | Event | Anatomy | Negation | Speculation | Pain term | Disease term |
Vitamin D receptor (VDR) transcription and protein levels were measured to examine whether VDR expression mediates differential regulation of duodenal TRPV6 between WT and KO mice, but expression and levels of VDR were similar in both genotypes. | |||||||||||||||
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Vitamin D receptor (VDR) transcription and protein levels were measured to examine whether VDR expression mediates differential regulation of duodenal TRPV6 between WT and KO mice, but expression and levels of VDR were similar in both genotypes. | |||||||||||||||
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Although the expressional changes were weak, duodenal expressions of glucocorticoid receptor (GR), the vitamin D receptor (VDR), and renal expressions of the parathyroid hormone receptor (PTHR) and VDR were increased following 24 h treatment with Dex. | |||||||||||||||
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Although the expressional changes were weak, duodenal expressions of glucocorticoid receptor (GR), the vitamin D receptor (VDR), and renal expressions of the parathyroid hormone receptor (PTHR) and VDR were increased following 24 h treatment with Dex. | |||||||||||||||
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The vitamin D receptor (VDR) is present in muscle cells, and the number of VDRs on each muscle cell appears to decrease with age [8]. | |||||||||||||||
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The vitamin D receptor (VDR) is present in muscle cells, and the number of VDRs on each muscle cell appears to decrease with age [8]. | |||||||||||||||
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The VDR-null mouse (lacking the VDR) has a phenotype characterized by reduced bone size, body size, weight, motor coordination, and poor physical performance compared with wild-type mice [11]. | |||||||||||||||
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The observed interaction between a CTR minor allele and the VDR C-A haplotype and their association with stress fractures may be explained by the inhibitory effect of these proteins on parathyroid hormone production. | |||||||||||||||
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Genotyping of 15 SNPs in the VDR, CTR, IL-6, COL1A1, COL1A2, and LRP5 genes | |||||||||||||||
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mediated Foxp3 was inhibited by 1,25(OH)2D3 via the VDR signal on CD4+ T cells (Figure 4). | |||||||||||||||
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Although the expressional changes were weak, duodenal expressions of glucocorticoid receptor (GR), the vitamin D receptor (VDR), and renal expressions of the parathyroid hormone receptor (PTHR) and VDR were increased following 24 h treatment with Dex. | |||||||||||||||
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Although the expressional changes were weak, duodenal expressions of glucocorticoid receptor (GR), the vitamin D receptor (VDR), and renal expressions of the parathyroid hormone receptor (PTHR) and VDR were increased following 24 h treatment with Dex. | |||||||||||||||
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However, the direct effect of 1,25(OH)2D3 on the function and differentiation of T cells is largely unknown because VDR is not expressed in naïve T cells [30]. | |||||||||||||||
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Vitamin D is a well-known nutrient that acts as a modulator of calcium homeostasis and the immune response [17], and the vitamin D receptor (VDR) is expressed in several types of immune cells, including monocytes, macrophages, dendritic cells (DCs), and effector/memory T cells [18][20]. | |||||||||||||||
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Thus, these inhibitory effects of 1,25(OH)2D3 are most pronounced in the effector/memory T cells which do express VDR or are mediated by 1,25(OH)2D3-treated DCs. | |||||||||||||||
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Vitamin D is a well-known nutrient that acts as a modulator of calcium homeostasis and the immune response [17], and the vitamin D receptor (VDR) is expressed in several types of immune cells, including monocytes, macrophages, dendritic cells (DCs), and effector/memory T cells [18][20]. | |||||||||||||||
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Although there is also a relatively high level of VDR expression in the small intestine, constitutive CYP24 expression in this tissue is very low or undetectable, in contrast to that in the kidney [Xu et al., 2006]. | |||||||||||||||
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Pascussi et al. first suggested that activation of SXR can enhance the expression of the VDR target gene, CYP24, which would increase the catabolism of 1,25(OH)2D3; thereby, leading to drug-induced osteomalacia [Pascussi et al., 2005]. | |||||||||||||||
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Here, we explored the mechanism of dietary protection by hCa by analyzing the expression of genes involved in the regulation of Ca uptake/flux in the intestinal epithelium, including the Ca-sensing receptor, vitamin D receptor, Ca binding protein, and transient receptor potential cation channels, subfamily V, members 5 and 6 (TRPV5/6). | |||||||||||||||
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Vitamin D is a well-known nutrient that acts as a modulator of calcium homeostasis and the immune response [17], and the vitamin D receptor (VDR) is expressed in several types of immune cells, including monocytes, macrophages, dendritic cells (DCs), and effector/memory T cells [18][20]. | |||||||||||||||
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