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Low Vitamin D receptor levels in breast cancer are linked to worse outcomes and more bone metastases, and could be a marker for prognosis.

ΔNp63α helps control a protein that stops cancer cells from spreading.

Stress activates a special function of the Vitamin D receptor with the help of c-Jun, which can also prevent cell death.

The R343H mutation in the VDR gene causes vitamin D-resistant rickets with alopecia by impairing specific gene activity.

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

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

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

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

A specific gene mutation causes vitamin D-resistant rickets and hair loss.

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.

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

A Chinese family had a child with a specific gene mutation causing vitamin D-resistant rickets, but the child improved with calcium and low-dose calcitriol.

VDR regulation varies by tissue and is crucial for its biological functions.

Mice without the vitamin D receptor have bone issues and other health problems, suggesting vitamin D is important for preventing various diseases in humans.

LEF1 interacts with Vitamin D Receptor, affecting hair follicle regeneration and this could be linked to hair loss conditions.

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

Removing the VDR gene in skin cells reduces their growth and affects hair-related genes.

The vitamin D receptor is crucial for bone health and affects various body systems, with mutations potentially leading to disease.

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

The review found no clear link between vitamin D receptor gene variations and polycystic ovary syndrome.

Certain gene variations in the Vitamin D receptor may increase the risk of chronic hair loss.

Patients with the same genetic mutation for vitamin D-resistant rickets showed different symptoms but all improved with treatment except for hair loss.

Two different mutations in the vitamin D receptor gene cause different symptoms and responses to treatment in Lebanese patients with hereditary rickets.

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

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

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

Two rare genetic diseases cause severe rickets in children due to defects in vitamin D metabolism.

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.

Vitamin D3 can help improve hair growth by enhancing the function of specific skin cells and could be useful in hair regeneration treatments.