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

A girl with type 1 diabetes developed a serious eye condition very early, suggesting the need for earlier eye checks and that early treatment can work well.

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

A woman's hair loss and other symptoms were due to a rare hormone deficiency treatable with steroids.

DPR can cause skin, hair, and nail issues, sometimes appearing later in life.

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

Certain enzymes react strongly with some hormones in rat skin during hair growth, mainly in sebaceous glands and hair sheaths.

The enzymes Aldh1a2 and Aldh1a3 are involved in making retinoic acid in hair follicles and have different roles in hair growth.

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.

Finasteride irreversibly affects human steroid 5α-reductase 2, providing insight into its catalytic mechanism and disease-related mutations.

A new enzyme in rats may help regulate hair growth.

The rs1128977 gene variant may affect cholesterol and body measurements.

4-(Ethoxycarbophenyl) retinamide is much less toxic than other retinoids.

A new genetic disorder caused by an ODC1 mutation can be treated with DFMO.

Lampreys have a functional vitamin D receptor that may help detoxify harmful substances.

A specific gene mutation causes vitamin D-resistant rickets and hair loss.

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

The enzyme 5α-reductase is important for proper blood vessel development during the fertility-related transformation of the uterus lining.

The human type II 5α-reductase gene has a specific structure important for understanding certain medical conditions.

Low ERCC3 gene activity is linked to non-pigmented hair growth.

Mice with a mutated Dsg3 gene showed severe symptoms but not the typical blistering of pemphigus vulgaris.

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.

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

Toll-like receptor 3 helps repair the skin barrier after UV damage.

Some people have genetic mutations that make them resistant to vitamin D, leading to rickets even with enough vitamin D intake.

Finasteride effectively inhibits the enzyme steroid 5 alpha-reductase II.

Patients with the same vitamin D receptor mutation showed different symptoms due to other factors.

A single amino acid change in the vitamin D receptor can disrupt its function and lead to hair loss.

Human liver enzyme DHEA ST helps process minoxidil.