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This study found that a novel R343H mutation in the vitamin D receptor gene impairs its transcription activity, contributing to hereditary vitamin D-resistant rickets and alopecia in the affected family.

This study found that Hairless (Hr) acts as a corepressor of the vitamin D receptor (VDR) in human keratinocytes, blocking the action of vitamin D on keratinocyte differentiation.

This study found that vitamin D receptor activation in primary keratinocytes can occur independently of the 1,25-dihydroxyvitamin D₃ ligand, likely through interaction with retinoid X receptors.

This study found that the protein hairless acts as both a corepressor and coactivator of the vitamin D receptor, influencing gene transcription in a ligand-selective manner.

This study identified a novel I268T mutation in the vitamin D receptor that reduces its function, contributing to hereditary vitamin D-resistant rickets, and found that a potent vitamin D analog could improve receptor function.