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

A gene mutation worsens skin irritation in mice due to a lack of certain fats.

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

Vitamin D receptor mutations can cause alopecia by affecting hair growth genes.

Hairless protein can block vitamin D activation in skin cells.

Mutations in the hairless protein gene cause hair loss.

The mutant HR bmh protein affects hair follicle formation by failing to repress vitamin D receptor activity.

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

A new gene mutation causes vitamin D-resistant rickets and hair loss in two siblings.

Mutations in the hairless gene in mice affect its expression and lead to a range of developmental issues in multiple tissues.

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

A mutation in the hairless gene speeds up severe itchy skin in mice on a special diet.

Two siblings with a genetic mutation had a form of rickets that doesn't respond to vitamin D.

The HR protein helps hair grow by blocking a hair growth inhibitor, aiding in hair follicle regeneration.

The mutant HR bmh protein mis-localizes in cells, affecting skin and hair development.

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

HVDRR is caused by VDR gene mutations, leading to vitamin D resistance, treatable with high calcium doses, but alopecia remains permanent.

The mutated hairless gene causes hair loss by acting as a new type of corepressor affecting thyroid hormone receptors.

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

The Hairless gene is crucial for healthy skin and hair growth.

A specific gene mutation is linked to a hereditary form of dystonia that responds well to certain medications.

Changes in the HR gene have influenced hair growth and may lead to hair loss conditions in humans.

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

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

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

Hairless protein helps control hair growth by regulating vitamin D receptor activity.

The hairless (hr) gene is essential for normal hair follicle function and its mutation leads to hair loss.

The Hr protein binds to DNA, interacts with p53, and affects cell cycle genes.

A new mutation in the Hr gene causes hair loss in mice, similar to a human hair disorder.