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The protein folliculin, involved in a rare disease, works with another protein to control how cells stick together and their organization, and changes in this interaction can lead to disease symptoms.

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

Mutant CDP/Cux protein causes hair defects and reduced male fertility in mice.

Lack of vitamin D receptor increases skin tumor risk by boosting hedgehog signaling.

VDR gene variations may affect carbohydrate metabolism in young women with hyperandrogenism.

Reduced TRPS1 leads to increased STAT3 and SOX9 in hair follicles, affecting hair growth.

Human cathepsin V can replace mouse cathepsin L to maintain normal skin and hair in mice.

The protein ER71/ETV2 helps regrow hair after chemotherapy by improving the growth of new blood vessels.

Trichothiodystrophy hair is structurally abnormal with protein and organization issues.

The mutation causes hairless mice due to mislocalized and dysfunctional HR protein.

Vitamin D receptor helps control skin cell growth and hair development.

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

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

Researchers created a mouse with the same mutation as humans with trichothiodystrophy, showing similar symptoms and confirming the condition is due to defects in DNA repair and gene activity.

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

Early detection of specific VDR mutations is crucial for effective treatment and better dental outcomes in children with hereditary vitamin D–resistant rickets.

Reduced Vitamin D receptor expression may cause hair loss through the Wnt/b-catenin pathway.

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

A gene mutation causes curly hair and hair loss in rats.

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

Three specific mutations in the LIPH gene can cause hair loss by damaging the protein's structure and function.

Vitamin D receptor gene variations are not linked to alopecia areata.

Mutations in the hairless protein gene cause hair loss.

Vaccines and targeting TrxR variants can help prevent cancer and reduce metastasis.

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

A variant in the ADAM17 gene causes hair loss by increasing protein degradation through TRIM47.

A new mutation in the TRPS1 gene was found in a Ukrainian girl with Trichorhinophalangeal syndrome type I.

Gene therapy with a vitamin D receptor gene improved hair growth in rats with a type of rickets-related baldness.

Repetin is a protein involved in skin and hair development, binding calcium and compensating for other proteins when needed.

A small change in the TRPS1 gene leads to a less severe form of a syndrome affecting hair, nose, and finger development.