Results: 3

1.
Figure 1.

Figure 1. From: The Nonskeletal Effects of Vitamin D: An Endocrine Society Scientific Statement.

A, Production of vitamin D from the skin via ultraviolet radiation (290–330 nm) in a nonenzymatic manner. B, The synthesis of vitamin D metabolites including the inactive form, 24,25-dihydroxyvitamin D, and the active form, 1,25-(OH)2D. This process is controlled at several levels, including the liver, kidney, and peripheral tissues, and is regulated by systemic hormones including PTH, 1,25-(OH)2D, and FGF23. Calcium and phosphorus are also major modulators of 1α-hydroxylase and 24,25-hydroxylase activity through their effects on PTH and FGF23. FGF 23, Fibroblast growth factor 23.

Clifford J. Rosen, et al. Endocr Rev. 2012 June;33(3):456-492.
2.
Figure 2.

Figure 2. From: The Nonskeletal Effects of Vitamin D: An Endocrine Society Scientific Statement.

Model of the VDR. The N-terminal region is short relative to other steroid hormone receptors. This region is followed by two zinc fingers, which constitute the principal DNA-binding domain. NLS are found within and just C-terminal to the DNA-binding domain. The LBD makes up the bulk of the C-terminal half of the molecule, with the AF-2 domain occupying the most C-terminal region. The AF-2 domain is largely responsible for binding to coactivators such as the SRC family and DRIP in the presence of ligand. Regions on the second zinc finger and within the LBD facilitate heterodimerization with RXR. Corepressor binding is less well characterized but appears to overlap that of coactivators in helices 3 and 5, a region blocked by helix 12 in the presence of ligand. NLS, Nuclear localization signals.

Clifford J. Rosen, et al. Endocr Rev. 2012 June;33(3):456-492.
3.
Figure 3.

Figure 3. From: The Nonskeletal Effects of Vitamin D: An Endocrine Society Scientific Statement.

Impact of vitamin D on the human innate (upper panel) and adaptive immune response (lower panel). When activated by mitogen or specific antigen, macrophages, dendritic cells, and lymphocytes express the VDR, thereby becoming targets for the active vitamin D metabolite, 1,25-(OH)2D. Macrophages and dendritic cells can also express the CYP27B1-hydroxylase that synthesizes 1,25-(OH)2D from substrate 25(OH)D, the major circulating metabolite of vitamin D and acknowledged best indicator of the amount of vitamin D entering the host via cutaneous synthesis or that ingested in the diet. Operating in an intracrine mode, 1,25-(OH)2D promotes microbial killing in the macrophage, whereas it inhibits maturation and the antigen-presenting capacity of the dendritic cell. If 1,25-(OH)2D escapes the confines of the macrophage or dendritic cell in sufficient amount, it can act on VDR-expressing lymphocytes recruited to the local inflammatory microenvironment. The major bioaction of 1,25-(OH)2D acting through the VDR in lymphocytes is to inhibit their proliferation and differentiation to maturity; this antiproliferative effect is more profound on the classes of helper than suppressor cells, leading to generalized suppression of the adaptive immune response. 1,25D, 1,25-dihydroxyvitamin D; 25D, 25-hydroxyvitamin D.

Clifford J. Rosen, et al. Endocr Rev. 2012 June;33(3):456-492.

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