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Two new enzymes, PAD-R11 and PAD-R4, were cloned and showed activity, with PAD-R11 resembling epidermal enzymes.

p63 and p73 regulate the vitamin D receptor, affecting cancer cell behavior and vitamin D sensitivity.

A gene deletion causes the "hairless" trait in Iffa Credo rats.

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

Ectodysplasin inhibits Wnt signaling to help form hair follicles.

Vitamin D Receptor is needed for hair growth in mice but not for skin stem cell maintenance.

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

As skin cells mature, vitamin D receptor levels decrease while retinoid X receptor α levels increase.

DDR-II hair follicle cells don't respond to 1, 25-dihydroxyvitamin D3, aiding diagnosis.

New SRD5A2 variants may disrupt protein function, aiding diagnosis and treatment of related disorders.

Alopecia in VDR knockout mice is due to impaired hair cycle initiation, not keratinocyte issues.

Most Recessive Dystrophic Epidermolysis Bullosa patients with a specific mutation likely have Sephardic ancestry from about 500 years ago.

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.

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

DEC cells show promise as a safe and effective treatment for Duchenne muscular dystrophy.

Alopecia in VDR knockout mice is due to a defect in hair cycle initiation, not keratinocyte issues.

VDUP1 is found in skin and hair follicles, interacts with sciellin, and may help regulate skin cell differentiation.

The enzyme Dgat1 is essential for healthy hair and skin by controlling retinoid levels.

Alopecia in these mice is caused by defective hair cycle communication due to missing vitamin D receptor function, not vitamin D levels.

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

DPR can show different hair characteristics, as seen in two brothers with normal hair.

Removing vitamin D and calcium receptors in mice skin cells slows down skin wound healing.

The PP2A-B55α protein is essential for brain and skin development in embryos.

ODC1 gene mutations cause a neurodevelopmental disorder with large head size, hair loss, and facial abnormalities.

The frizzy mouse and hairless rat mutations are due to changes in the Prss8 gene.

The most common sign of aging at the gene level is more Ectodysplasin A2 Receptor (EDA2R) being made.

Mice lacking steroid 5α-reductase 2 show less aggression and better impulse control.

Ptprq has multiple forms that change during inner ear development.

TEDAR is crucial for skin cell differentiation and barrier formation.

Vitamin D receptor FokI gene variation is not linked to alopecia areata.