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This study found that the effects of the vitamin D receptor on hair follicle cycling in mice are independent of its ability to bind a hormone, with specific domain mutations influencing hair regrowth outcomes.

This study found that hair follicle homeostasis in mice requires vitamin D receptor expression in keratinocytes, independent of its ligand activation.

This review presents updated tables of mouse mutants with hair growth abnormalities to aid in understanding the molecular mechanisms of human hair disorders, but reports no new clinical results.

This study found that most pathogenic HR mutants associated with atrichia with papular lesions had abolished corepressor activity due to defective interactions with histone deacetylases.

This study found that humanized mouse models expressing mutated or reduced levels of the vitamin D receptor were able to maintain normal mineral homeostasis and prevent typical symptoms of vitamin D resistance.