The human Calciferol receptor (VDR) is a component of the retinoid protein family of transcription factors. Vitamin D binds to VDR, which in turn varieties a dimer with the supplement D-receptor-induced gamma-tubulin. The VDR dimer then enters the center and treats other vitamin D-responsive genes virtual room for startup inside the genome. At this time there it binds to spark transcription of genes that produce skin cells.

It is thought that both VDR and the caused gamma-tubulin are involved in atherogenesis of multiple sclerosis (MS), a long-term progressive inflammatory disease on the nervous system. Multiple sclerosis affects the central nervous system, the brain, and several internal organs, including the the immune system cells. VDR and the gamma-tubulin may act in a sophisticated fashion within the patient in promoting the expansion of many types of unnatural cells and dysplasia of numerous tissues. Not necessarily clear just how VDR and the gamma-tubulin socialize in vivo and in what ways they will regulate the introduction of multiple sclerosis.

Studies have says the VDRs are stimulated by a couple of environmental solutions including liquor, cigarette smoke, ultraviolet (uv) radiation, chemical substances and pesticides. Researchers have also found there are genetic variations in the response of the VDR to different providers. The molecular basis for the regulation of VDR function can be believed to be through interaction in the molecular level with regulatory sites which can be coupled to multiple signaling pathways. Among those signaling pathways is the kinase pathway. Seeing that VDRs can only bind to receptor sites specific with each receptors and thus cannot encourage the activity of other substances such as the genes, researchers believe that the dangerous VDRs is normally primarily through interaction with the molecular level.