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Intravenous calcium therapy is a safe and effective treatment for a rare type of rickets.

Vitamin D is made by the skin, helps control various body functions, and affects skin health and immunity.

Researchers created a mouse model of a type of rickets that does not cause hair loss.

Vitamin D receptor is crucial for skin wound healing.

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

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

Removing part of the vitamin D receptor stops vitamin D from working properly.

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

Mice without the vitamin D receptor gene lose hair due to disrupted hair follicle cycles.

Vitamin D receptor interacts with certain dietary components to help prevent diseases and regulate hair growth.

Basal cell carcinomas have much higher levels of Vitamin D3 receptors compared to healthy skin.

Vitamin D receptor is crucial for bone health and mineral metabolism.

Vinblastine and its metabolites may cause nausea and hair loss by binding to specific receptors and could lead to better chemotherapy drugs with fewer side effects.

Vitamin D is important for skin cell growth and health, and its active form and receptor play key roles in skin and hair processes.

Skin cells produce and activate vitamin D, which regulates skin functions and supports hair growth.

The vitamin D receptor is involved in multiple body functions beyond calcium regulation, including immune response and rapid reactions not related to gene activity.

Nuclear hormone receptors play a significant role in skin wound healing and could lead to better treatment methods.

KLF4 is important for keeping hair follicle stem cells inactive.

Most Hairless gene mutations reduce its ability to work with the Vitamin D Receptor, which might explain a certain type of hair loss.

Targeting the Wnt pathway might help treat hair loss.

Vitamin D receptor may help protect against UV-induced skin cancer.

The vitamin D receptor is essential for skin stem cells to grow, move, and become different cell types needed for skin healing.

Vitamin D affects Msx1 protein expression and may influence mineralized tissue health.

The skin produces and uses vitamin D for bone health, cell growth, and immune function.

Mice without Vitamin D receptors have hair growth problems because of issues in the hedgehog signaling pathway.

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

Hairless protein can both repress and activate vitamin D receptor functions, affecting gene regulation.

People with alopecia areata often have lower vitamin D levels, which are linked to more severe and longer-lasting hair loss, but vitamin D receptor levels in the skin don't show the same pattern and don't predict treatment success.

Vitamin D receptor binds similarly to natural and synthetic ligands, affecting gene regulation.

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