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This study found that keratin K17 is induced in the suprabasal layer of psoriatic scalp epidermis during epidermal hyperproliferation, suggesting it is not specific to hair follicles.

In this study, researchers found that selectively disabling ribonucleotide excision repair in mouse epidermis caused DNA damage, skin inflammation, and led to skin cancer, suggesting a potential role for this repair mechanism in tumorigenesis.

This study found that COL17 deficiency in neonatal mice causes abnormal skin cell proliferation due to disrupted Wnt signaling, while replenishing or overexpressing COL17 can reverse this effect in both neonatal and aged skin.

This study found that EGF receptors are aberrantly regulated and persist in cholesteatoma epithelium, suggesting a hyperproliferative character compared to normal human skin.

This study found that overexpression of PKCepsilon in transgenic mice reduced papilloma development but accelerated carcinoma formation in a skin tumor promotion model.

This study found that activating the erbB-2 oncogene in transgenic mice led to severe skin abnormalities and fatal defects, indicating erbB-2's significant role in skin and hair follicle development.

The study concluded that fatty acid transport protein 4 in epidermal keratinocytes is crucial for maintaining normal skin structure, as its deficiency led to hyperkeratosis and epidermal barrier disruption in mice.

This study identified that the Wave complex proteins ABI1 and Wave2 play a crucial role in regulating epidermal shape and growth during skin development, notably influencing SOX9 expression and Wnt signaling pathways.

This study found that in a transgenic mouse model, β-HPV infection led to increased skin thickness and proliferation of specific keratinocyte stem cells, which may contribute to squamous cell carcinoma development.

HDAC1 is crucial for skin development and preventing tumors.

This study demonstrates that overexpression of K16 in transgenic mice disrupts normal keratinization, leading to hyperkeratosis, acanthosis, and alterations in the skin's epithelial cells.

This study found that Nrf2 activation protected keratinocytes from UVB damage but also caused thickening, inflammation, and cysts, limiting its therapeutic potential for skin protection.

This study found that abolishing H3K27me3 in mouse skin by targeting Ezh2 and Ezh1 affects hair follicle development and epidermal behavior, revealing functional differences between these tissues.

This study suggests that vitamin D and its receptor may protect against the development of epidermal tumors following UV radiation by regulating specific cellular signaling pathways.

This study found that deleting the Twist1 gene in skin keratinocytes significantly reduced UVB-induced skin cancer and hyperproliferation in mice and suggested Twist1 as a target for skin cancer prevention.

This study found that deleting β-catenin in epidermis-specific VDR knockout mice did not prevent UVB-induced skin tumors, indicating β-catenin does not compensate for VDR's role in tumor suppression.

In this study, activation of c-MycER in adult mouse epidermis rapidly induced proliferation and disrupted keratinocyte differentiation, causing changes similar to precancerous lesions, which regressed once c-MycER was deactivated.

In a transgenic mouse model, this study found that overexpression of keratin 16 in skin keratinocytes led to hyperkeratosis and increased EGF receptor signaling, altering skin cell behavior and structure.

This study identified a missense mutation in the rat Desmoglein 4 gene, causing abnormal hair shaft development in lanceolate hair mutant rats by disrupting a critical calcium binding site.

This study found that high levels of human cytokeratin 16 expression in transgenic mice lead to skin lesions and altered keratinocyte structure, suggesting potential implications for human skin disorders and wound healing.

Lack of vitamin D receptor increases skin tumor risk by boosting hedgehog signaling.

This study found that bulge keratinocytes in mice develop resistance to glucocorticoid treatment more slowly than interfollicular keratinocytes and do not significantly aid in repairing glucocorticoid-induced skin atrophy within five days.

This article discusses the roles of epidermal stem cells in maintaining skin homeostasis and highlights how deregulation in signaling pathways may lead to cancer, but it reports no new experimental results.

This study found that, in mouse tail epidermis, stem cells rapidly activate and regenerate new progenitors to repair wounds, with mechanisms affecting their proliferation, differentiation, and migration.

This study found that RXRα/RARγ heterodimers are necessary for retinoic acid-induced keratinocyte proliferation in the skin, while normal epidermal maintenance does not require RAR-mediated signaling.

This study found that disrupting Smad4 signaling in young mice led to overactivation of follicle stem cells, causing hyperplasia and depletion of the stem cell niche.

This study established that a human epidermal model can be utilized to assess 5alpha-reductase activity and evaluate enzyme modulators, such as finasteride, for dermatological applications.

This study found that Ift20 is essential for hair follicle stem cell identity and hair regrowth, and it regulates keratinocyte migration during wound healing through focal adhesion integrin recycling, independently of ciliogenesis.

In this study, inactivating the TAF4 subunit of transcription factor TFIID in mouse epidermis disrupted gene expression linked to skin and hair function, and increased tumor risk.

This article reviews current research on epidermal stem cells and differentiation, presenting models of basal layer composition, but reports no new experimental findings.