Sandbox Reserved 428: Difference between revisions
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==Introduction== | ==Introduction== | ||
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The vitamin D receptor(VDR) is ligand-dependent transcriptional regulator. VDR belongs to the superfamily of nuclear receptors which control homeostasis, cell differentiation and growth, and many physiological processes. All proteins that belong to the nuclear receptor superfamily have a variable N-terminus region (A/B region), a hinge region that is flexible (D region), a conserved DNA-binding region (DBD, C region), and a moderately conserved ligand-binding region (LBD, E/F region). In the case of VDR, the R/B region is very short so it does not have any AF-1 function and the ligand binding region has a dimerization interface and a transcriptional activation domain that is ligand-dependent (AF-2).[1] <br><br> | |||
The VDR has both an active and suppressed form. The activation or suppression function is caused by the binding of the DR3 response element as a heterodimer with the retinoid X receptor of the target genes. Due to the interactions with the basal transcriptional machinery and transcriptional cofactors, transcription is either activated or suppressed. When VDR is in its active form it regulates both phosphate and calcium metabolism, has immunosuppressive effects, and induces cell differentiation. When there are defects in the VDR that effect its metabolism it can lead to diseases such as severe rickets, secondary hyperparathyroidism, and hypocalcemia. Though defects in VDR can cause many diseases, fully functioning VDR can be used as treatment for disease such as cancer, autoimmune disease, psoriasis, osteoporosis, and renal osteodystrophy.[1] | |||
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