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- Smad7-Induced β-Catenin Degradation Alters Epidermal Appendage Development
- Human bone marrow mesenchymal stem cell-derived exosomes stimulate cutaneous wound healing mediates through TGF-β/Smad signaling pathway
- Overexpression of Smad7 results in severe pathological alterations in multiple epithelial tissues
- Bone morphogenetic protein-2 (BMP-2) transactivates Dlx3 through Smad1 and Smad4: alternative mode for Dlx3 induction in mouse keratinocytes
- The 800-nm diode laser irradiation induces skin collagen synthesis by stimulating TGF-β/Smad signaling pathway
- The Role of Smads in Skin Development
- Disruption of Smad4 in Mouse Epidermis Leads to Depletion of Follicle Stem Cells
- Smad1 and 5 but Not Smad8 Establish Stem Cell Quiescence Which Is Critical to Transform the Premature Hair Follicle During Morphogenesis Toward the Postnatal State
- Smad4-dependent desmoglein-4 expression contributes to hair follicle integrity
- Androgen receptor transactivity is potentiated by TGF-β1 through Smad3 but checked by its coactivator Hic-5/ARA55 in balding dermal papilla cells
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