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A new gene mutation causes vitamin D resistance and rickets, treatable with calcium therapy.

Vitamin D receptor knockout mice have significant motor impairments but no cognitive deficits.

PPAR alpha may help in hair growth and could be a target for treatment.

Fatty acid composition in human skin, mouth, and hair cells varies with keratinization, and cultured cells show essential fatty acid deficiency.

A specific gene mutation causes congenital hair loss.

Gene therapy helped rats with a specific type of rickets grow hair without severe inflammation.

The vitamin D receptor can work without its usual activating molecule.

Mice without the vitamin D receptor are more prone to UV-induced skin tumors.

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

Vitamin D receptor is crucial for hair health and may help treat hair loss.

Mutations in the Vitamin D receptor gene can cause hair loss similar to mutations in the Hairless gene.

The vitamin D receptor can regulate genes and affect hair and hormone levels without its usual activator.

Non-liganded Vitamin D Receptor is crucial for healthy skin and hair.

Vitamin D Receptor is needed for hair growth in mice but not for skin stem cell maintenance.

Ferulic acid helps wounds heal faster by reducing inflammation and promoting skin cell movement.

Vitamin D Receptor is crucial for normal skin and hair growth.

Vitamin D receptor is crucial for normal hair growth and preventing hair loss.

Increasing calcium sensing receptor speeds up skin and hair development in mice.

Thyroid hormone receptors are essential for hair growth and wound healing.

Endothelial TLR2 is crucial for timely wound healing, but HFSC TLR2 is not needed.

Hyaluronic acid hydrates and benefits skin and hair safely.

The gel is a safe and effective treatment for hyperpigmentation.

Ursolic acid may help develop new anti-inflammatory drugs by affecting immune cells.

Azelaic acid helps protect hair cells from UV damage and encourages hair growth by increasing certain gene expressions and proteins.

Hairless protein can block vitamin D activation in skin cells.

Mutations in the vitamin D receptor cause hereditary vitamin D-resistant rickets, leading to poor bone health and requiring high calcium doses for treatment.

Certain gene variations in the Vitamin D Receptor are linked to higher risk of female hair loss.

Human keratinocytes do not naturally respond to androgens.

Transferrin receptor expression increases iron in mouse skin cells without causing damage.

Lack of TrkC receptor delays hair follicle development.