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Folliculin deficiency causes problems with cell division and positioning due to disrupted RhoA signaling and interaction with p0071.

Artemis phosphorylation at Ser516 may help regulate skin and hair structures.

The study concluded that PKP1 is essential for skin integrity and hair growth, and its dysfunction causes the symptoms of ectodermal dysplasia/skin fragility syndrome.

A specific gene mutation causes a severe skin disorder in a family.

Trps1 is essential for proper hair follicle development.

TRPV3 in skin cells causes inflammation and cell death.

GPRC5D is linked to the formation of hair, nails, and certain tongue areas.

A new genetic mutation in the TRPS1 gene causes Trichorhinophalangeal Syndrome, leading to specific hair, dental, and bone issues.

Human hair keratin genes have unique simple sequence repeats that may help track genetic variations.

Trps1 plays a key role in hair follicle development and cycling.

Anti-Ku-positive patients often have muscle weakness and autophagy plays a key role in their condition.

Spt4 and Spt6 are essential for fat cell development.

TRPV3 channels are involved in skin processes and are affected by shear stress, influencing itch and mechanotransduction.

Activating cannabinoid receptor 1 may help manage psoriasis by reducing certain keratins.

AGD1's PH domain is essential for its role in root hair growth and polarity.

Keratin 17 is crucial for normal hair growth by regulating hair cycle transitions with TNFα.

DermaCult™ Keratinocyte Expansion Medium allows human skin cells to grow longer while keeping their ability to develop properly.

TRPA1 is crucial for mechanical sensitivity in skin sensory neurons.

A new keratin, hK6irs1, is found in all layers of the hair follicle's inner root sheath.

KAP-depleted hair causes less immune response and is more biocompatible for implants.

A Korean girl developed kinky hair without known cause or effective treatment.

Reptile skin hardens by layering beta-proteins on keratin.

SPT6 prevents excessive skin inflammation by blocking a feedback loop.

The NIPAL4 mutation c.527C>A is common in Romanian patients with autosomal recessive congenital ichthyosis.

Human keratinocytes do not naturally respond to androgens.

Junctional proteins stabilize the inner root sheath and connect the companion layer in human hair.