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Four patients with a type of rickets and hair loss had different mutations in their vitamin D receptor gene, causing it to not work properly.

Vitamin D is crucial for bone health and preventing serious diseases.

Vitamin D receptor is important for regulating hair growth and wound healing in mice.

Certain mutations in the hairless protein disrupt its ability to regulate the hair cycle.

The vitamin D receptor can affect gene activity even without its usual hormone in hair and skin.

Targeting the Wnt pathway might help treat hair loss.

Expressing the human vitamin D receptor in skin cells prevents hair loss in certain mice.

A single amino acid change in the vitamin D receptor can disrupt its function and lead to hair loss.

Low vitamin D receptor levels found in hair loss patients; topical vitamin D treatment suggested.

Vitamin D boosts a specific protein in skin cells linked to hair follicles.

The vitamin D receptor helps regulate skin and hair health independently of its usual vitamin D ligand.

Different Hairless isoforms affect Vitamin D receptor activity in hair regulation, with one repressing and the other stimulating it.

A genetic mutation caused severe rickets and alopecia in an Indian patient, but high-dose calcium and phosphate treatment improved their condition.

Lack of Vitamin D receptor changes skin structure and increases certain immune cells in the skin.

Vitamin D and calcium are important for quick and effective skin wound healing.

As skin cells mature, vitamin D receptor levels decrease while retinoid X receptor α levels increase.

Vitamin D3 may protect rat hair follicles from radiation damage.

Vitamin D and calcium are important for skin stem cell function and wound healing.

Mice without active or present vitamin D receptors maintain normal blood sugar control and islet gene expression when calcium levels are normal.

Vitamin D receptor helps control hair growth genes in skin cells.

Vitamin D receptor gene variations are not linked to alopecia areata.

A vitamin D receptor mutation causes rickets and affects immune responses.

Combining skin tissue pathology with genetics has greatly improved the diagnosis and understanding of certain skin diseases.

Early detection of specific VDR mutations is crucial for effective treatment and better dental outcomes in children with hereditary vitamin D–resistant rickets.

The vitamin D receptor can act without its usual activating molecule, affecting hair growth and skin cancer, but its full range of actions is not well understood.

Three new gene mutations cause rickets and hair loss, treatable with high calcium and calcidol, but hair regrowth is rare.

Vitamin D receptor can control the hairless gene linked to hair loss even without vitamin D.

Vitamin D receptor FokI gene variation is not linked to alopecia areata.

Vitamin D receptor helps protect skin cells from UV damage and supports their growth.

New mutations in the VDR gene cause vitamin D-resistant rickets without hair loss.