VDR functions play a significant role in the development, metabolism and homeostasis. Vitamin-D/VDR is involved in numerous other biological processes, like the immune system’s control, cell reproduction and gene expression in addition to its traditional function in controlling the absorption of calcium into the intestinal tract and bone tissue.
When liganded by RXR, VDR forms homodimers or heterodimers, and triggers transcription through binding to DNA response element. This process is influenced a by the interaction between the ligand binding domain (LBD), and the heterodimerization area. Natural mutations to the LBD in VDR cause a vitamin D resistance phenotype. Mutagenesis studies have demonstrated that there are areas in the LBD that are critical for heterodimerization.
Unliganded VDR interacts with regulatory regions in cWnt and Sonic hedgehog gene promoters. This interaction is crucial to the induction of these pathways during the postnatal hair cycle. Inhibition of VDR-b-catenin interaction by 1,25(OH)2D3 results in the repression of the expression of these genes.
VDR-null mice have a behavioral characteristic that is characterized as impaired balance and motor function and a decline in the capacity to perform the swimming test. The phenotype is caused by https://dataroomapps.net/data-management-made-simple-how-virtual-data-rooms-can-simplify-your-complex-business-processes a disruption in the cellular expression of a range of cytoskeletal proteins, such as actin and myofilaments. Immunohistochemistry tests have shown that these protein changes are associated with a decrease in myofilaments, and a reduced fiber diameter.