Abstract
Smad7 structurally consists of N- and C- terminal domains linked with a PY motif. It shuttles between nuclear and cytoplasm to exert different biological functions. Smad7 was overexpressed in epidermis of clinical psoriatic lesions, which was thought to contribute to epidermal hyperplasia in psoriasis. To address if this is the case, we assessed the role of Smad7 and its functional domains in IMQ-induced psoriatic pathogenesis using genetic and pharmacological approaches. K5.Smad7 mice, which express Smad7 transgene(Tg) by a keratin-5 promoter, were resistant to IMQ-induced psoriatic lesions, suggesting an anti-inflammatory effect of Smad7 overexpression.
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