The postnatal hair cycle is regulated by the vitamin D receptor. VDR deficiency could cause various health issues, such as backache joints, joint pain and the development of rickets.
The vitamin D receptor also plays an important role in bone development regulation. Correlation between bone density in humans and VDR receptor variants in them suggests the function of this receptor. A small portion of glial cells recognize the receptor. This is connected to the growth of white matter of glial fibrillary acidic protein (GFAP).
A variety of protein kinases phosphorylate the VDR at serine residues. These interactions could modify its function or improve its interaction with coactivators.
VDR is expressed in several cells of the body, including platelets, neutrophils, dendritic cells (DCs) and macrophages. The human brain is the most affected, and the VDR is believed to be present in some glia.
Vitamin D response elements regulate the activity of vitamin D-responsive genes, including the genes that produce calcium-binding proteins calbindin D-9k and vdr 12-O-tetradecanoylphorbol-13-acetate (TPA). Several genes have been identified as potential targets to the VDR.
Vitamin D activates VDR and makes heteromers (VDR) together with the retinoid-X receptor (RXR). VDR triggers and produces a complex that contains vitamin D’s active ingredient and the calcitriol. The complex then relays the signal through hydrogen-deuterium exchange.
A VDR allele is linked to a higher risk for low vitamin D levels. It’s also linked with osteoporosis, rickets and backache.