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Tunisian children with hereditary vitamin D-resistant rickets showed improvement with calcium treatment, and new genetic mutations were identified.

A unique gene mutation causes vitamin D-resistant rickets without causing hair loss.

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.

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

Mutations in the hairless protein gene cause hair loss.

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

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

A rare genetic mutation causes resistance to vitamin D, leading to severe rickets and requiring high doses of calcium and vitamin D for treatment.

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

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

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

The vitamin D receptor is essential for normal hair growth, even without its usual binding.

Vitamin D receptor and hairless protein are essential for hair growth.

The research showed that Vitamin D and its receptor are important for healthy bones and normal hair and skin in rats.

Vitamin D receptor is crucial for hair growth, not vitamin D itself.

Vitamin D receptor helps prevent skin tumors.

Hairless protein can block vitamin D activation in skin cells.

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

The vitamin D receptor can act without its usual activating molecule, affecting hair growth and skin cancer, but its full range of actions is not well understood.

The vitamin D receptor helps maintain hair and bone health even without binding vitamin D.

VDDR I and II are genetic disorders affecting vitamin D use, causing rickets, with VDDR I treatable by vitamin D supplements and VDDR II needing high doses and calcium.

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

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

Combining skin tissue pathology with genetics has greatly improved the diagnosis and understanding of certain skin diseases.

Retinoic acid affects skin and hair health by working with specific receptors, and its absence can lead to hair loss and skin changes.

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

A rare genetic mutation causes resistance to vitamin D, leading to severe rickets and requires high doses of calcium and vitamin D for management.

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

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

Certain VDR gene changes can affect melanoma risk.