Smad7-Induced Beta-Catenin Degradation Alters Epidermal Appendage Development

    September 2006 in “ Developmental Cell
    Gangwen Han, Allen G. Li, Yao-Yun Liang, P. C. Owens, Wei He, Shi‐Long Lu, Yasuhiro Yoshimatsu, Donna Wang, Peter ten Dijke, Xia Lin, Xiaojing Wang
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    TLDR Too much Smad7 changes skin and hair development by breaking down a protein called β-catenin, leading to more oil glands and fewer hair follicles.
    The study from 2006 explored how Smad7 affects skin development, particularly hair follicle formation and sebaceous gland development, in transgenic mice. It was found that Smad7 overexpression disrupted hair follicle morphogenesis and differentiation, while accelerating sebaceous gland development. This was due to Smad7 binding to β-catenin and inducing its degradation by recruiting the E3 ligase Smurf2, which suppressed Wnt/β-catenin signaling. The abnormalities in hair follicles and sebaceous glands were exacerbated when Smurf2 and Smad7 were co-expressed. Conversely, reducing Smad7 levels in keratinocytes increased β-catenin protein and Wnt signaling. The study concluded that Smad7 antagonizes Wnt/β-catenin signaling, which alters the skin differentiation program, favoring sebaceous gland formation over hair follicles. The number of mice used in the study was not specified.
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