Increased Expression of Keratin 16 Causes Anomalies in Cytoarchitecture and Keratinization in Transgenic Mouse Skin

The study found that overexpression of the human K16 gene in transgenic mice led to abnormal keratinization in the hair follicle outer root sheath and proximal epidermis, resulting in hyperproliferation and increased thickness of both living and cornified skin layers. This was due to a reorganization of keratin filaments in postmitotic keratinocytes, which disrupted keratinocyte cytoarchitecture and altered desmosomes. The findings suggested that high levels of K16, along with K6 and K17, could reorganize keratin filaments, interfering with normal terminal differentiation in skin epithelial cells.