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This study found that loss of epidermal PPARγ in mice altered the expression of many genes related to skin inflammation, keratinization, and sebaceous gland function, indicating its key role in maintaining skin homeostasis.

This study found that loss of the DNA methyltransferase Dnmt3a, but not Dnmt3b, increased carcinogen-induced squamous tumors in murine epidermis, with combined deletion leading to more aggressive and metastatic carcinomas.

The research found that while Dnmt3a and Dnmt3b are not necessary for skin homeostasis in mice, the loss of Dnmt3a increases squamous tumor formation from carcinogens, and combined deletion of both results in more aggressive and metastatic tumors.

This study suggests PPAR isotypes play distinct roles in skin, influencing epidermal barrier formation, sebocyte differentiation, and lipid production, with potential implications for treating skin disorders.

This study observed that inducible deletion of the Ugcg gene in mouse epidermis led to a significant reduction in GlcCers and epidermal POS-Cers, causing impaired skin barrier function and delayed wound healing.