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

Hairless protein can block vitamin D activation in skin cells.

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

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

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

Certain defective glucocorticoid receptor mutants move faster inside cell nuclei and work less effectively.

NcoA4 may have roles beyond helping control gene activity, possibly affecting cell behavior and stability.

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

Mutations in the androgen receptor gene cause different levels of androgen insensitivity, making it hard to create simple tests for the condition.

Researchers found new potential treatments for conditions related to the androgen receptor, like male hormonal contraception, by testing thousands of compounds.

DHEA affects various tissues by interacting with multiple receptors and can be converted into sex hormones.

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.

A new mutation in the human glucocorticoid receptor reduces its function and causes resistance to glucocorticoids.

Madarosis is the loss of eyelashes and eyebrows due to various health issues and requires thorough examination to diagnose and treat the underlying cause.

Hairless protein affects hair follicle structure by regulating the Dlx3 gene.

Hormones and neuroendocrine factors control hair growth and color, and more research could lead to new hair treatment options.

Deleting MED1 in skin cells causes hair loss and skin changes.

MED1 is essential for normal hair growth and maintaining hair follicle stem cells.

B6.Cg-Tyr c−2J Hr hr /J mice have a stronger delayed sunburn reaction and are good for UV research.

Melatonin affects many body functions beyond sleep by interacting with specific receptors in various tissues.

Hair follicles are hormone-sensitive and involved in growth and other functions, with potential for new treatments, but more research is needed.

Fadrozole and finasteride change gene expression related to sex hormones and thyroid hormones in frog larvae development.

The skin acts like an endocrine organ, producing hormones that affect various body functions and skin health, and understanding this can lead to new treatments.

5α‐reductase isozymes are crucial for prostate development and health, and targeting them can help prevent and treat prostate issues.

Using neurohormones to control keratin can lead to new skin disease treatments.

Hormonal interactions, especially involving DHT and estrogen, play a key role in BPH development and treatment.

Damaged hair follicles make mice more prone to skin inflammation and skin cancer after UV exposure.

Jumonji genes are important for development and their mutations can cause abnormalities, especially in the heart and brain.

Thyroid receptor β can help develop new drugs to treat hair loss.