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• W2274163845 abstract "Non-melanoma skin cancer is the most commonly diagnosed cancer in the United States. The cause of most non-melanoma skin cancer is prolonged exposure to UVirradiation. UV-irradiation acts as both an initiator and tumor promoter, possibly through its activation of receptor tyrosine kinases (RTKs) such as the members of the Erbb family. Erbb2, an orphan receptor and member of the Erbb family, was recently demonstrated to be involved in the regulation of cell cycle progression after UV-induced DNA damage. This report describes the use of a skin-targeted conditional Erbb2 null mouse (to be referred here as an Erbb2 mutant mouse) to study Erbb2’s role in the skin’s response to UV-irradiation. Using this model, the effects of Erbb2 on cell cycle progression, DNA damage repair, and mutagenesis were analyzed after UV-irradiation. Surprisingly, Erbb2 mutant skin lacks a UV-induced S-phase arrest observed in previous studies utilizing the Erbb2 inhibitor AG825, suggesting that Erbb2 mutant skin compensates for its loss of Erbb2. However, Erbb2 reduces the efficiency of DNA damage repair and increases clonal expansion of keratinocytes with Trp53 mutations through mechanisms independent of its regulation of the cell cycle after UV-irradiation. These results suggest that erbb2 may contribute to skin carcinogenesis through multiple mechanisms." @default.
• W2274163845 created "2016-06-24" @default.
• W2274163845 creator A5056960499 @default.
• W2274163845 date "2008-05-20" @default.
• W2274163845 modified "2023-09-26" @default.
• W2274163845 title "Erbb2: A Regulator of the Skin's Response to Ultraviolet Radiation" @default.
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