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The research suggests that a specific skin gene can be controlled by signals within and between cells and is wrongly activated in certain skin diseases.

Too much keratin 16 in mice skin causes abnormal skin thickening and structure.

The peach gene CTG134 helps control the interaction between auxin and ethylene, which could lead to new agricultural chemicals.

NCSTN gene mutation causes abnormal skin cell differentiation and more inflammation, contributing to Hidradenitis Suppurativa.

The B2C promoter works in sheep cells but not in mouse embryos.

AP-1 and TGFß work together to drive resistance in basal cell carcinoma, suggesting new treatment options.

Disrupting Acvr1b in mice causes severe hair loss and thicker skin.

A protein called PCBP2 controls the production of a hair growth protein by interacting with its genetic message and is linked to hair loss when this control is disrupted.

UTX is crucial for skin differentiation and health, especially in females.

Plasmalogens activate a channel in cells that may stimulate hair growth.

Wnt3a activates certain genes in hair follicle cells, including a newly discovered one, EP2, which may affect hair growth.

Overexpressing COX-2 in mice skin reduces skin tumor development.

A new gene mutation linked to Olmsted syndrome may increase cancer risk, suggesting the need for ongoing patient monitoring.

Overactive Wnt5a disrupts hair follicle orientation in mice.

Scientists identified three genes important for processing certain brain chemicals, thyroid hormones, and medications.

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

Targeting the p300/AR axis may help treat polycystic ovary syndrome.

The protein p53 directly reduces the production of Keratin 17, a skin and hair protein, in rats with radiation dermatitis.

HPV8 causes hair follicle stem cells to grow, leading to skin lesions.

All-trans-retinoic acid stops mink hair growth by affecting cell growth and causing cell death.

Testosterone in our bodies helps increase insulin secretion from the pancreas.

Defective nuclear transport may cause gene expression changes in Progeria.

Loss of the p53 gene alone causes tumors, and losing both p53 and Rb genes speeds up aggressive skin cancer.

Certain gene variations in the Vitamin D receptor may increase the risk of chronic hair loss.

Noggin overexpression delays eyelid opening by affecting cell death and skin cell development.

Vitamin D receptor and hairless protein are essential for hair growth.

Increasing calcium sensing receptor speeds up skin and hair development in mice.

Twist1 helps maintain important features of cells crucial for hair growth by working with Tcf4 and β-catenin.

Adding a second method to PROTACs could improve cancer treatment.