The Vitamin D Receptor Functions as a Transcription Regulator in the Absence of 1,25-Dihydroxyvitamin D3
August 2015
in “
The Journal of Steroid Biochemistry and Molecular Biology
”
New to cholecalciferol? There is a guide in the encyclopedia. Read the guide → Studysummary This study found that in a mouse model with hereditary 1,25-dihydroxyvitamin D resistant rickets, a mutant vitamin D receptor lacking hormone-binding ability could restore normal hair cycling and affect parathyroid hormone regulation. Our plain-language summary of this paper — not a Tressless recommendation.
The study explored the role of the vitamin D receptor (VDR) in the absence of its ligand, 1,25-dihydroxyvitamin D3 (1,25(OH)2D3), particularly in hair cycling and parathyroid hormone (PTH) regulation. Using mouse models, researchers found that VDR could facilitate normal hair cycling without 1,25(OH)2D3, suggesting a ligand-independent function. Additionally, VDR appeared to influence PTH secretion independently of 1,25(OH)2D3, as evidenced by higher PTH levels in Cyp27b1 null mice compared to VDR null mice. This indicated that VDR might act as a selective suppressor or de-repressor of gene expression without its ligand, affecting tissues beyond the skin.