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The early genes of a specific virus can cause abnormal skin cell growth and hair follicle changes.

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

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

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

Trichothiodystrophy hair is structurally abnormal with protein and organization issues.

Certain mutations in a hair growth-related gene cause a type of genetic hair loss.

TRPV1 helps regulate hair growth cycles.

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

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

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

The environment around the time of conception can change the VTRNA2-1 gene in a way that lasts for years and may affect disease risk.

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

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

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

Mutations in the hairless protein gene cause hair loss.

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

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

TRPV4 slows hair growth by affecting hair follicle cells.

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

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.

Three new gene mutations cause rickets and hair loss, treatable with high calcium and calcidol, but hair regrowth is rare.

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

Carriers of a specific gene mutation have subtle skin changes without visible symptoms.

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

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

The Trichodysplasia spinulosa virus protein can cause abnormal hair growth in mice.

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

The vitamin D receptor can affect gene activity even without its usual hormone in hair and skin.

Deleting the Trf1 protein in mice is safe and may help prevent cancer without major side effects.

Researchers found a non-functional sheep keratin gene due to mutations.