Keratin 17 null mice exhibit age- and strain-dependent alopecia

The study on Keratin 17 (K17) null mice revealed that these mice developed severe alopecia within the first week after birth, linked to hair fragility, changes in follicular histology, and apoptosis in matrix cells. These effects were not fully penetrant and began to normalize with the first postnatal cycle. The absence of a hair phenotype was associated with genetic strain-dependent compensation by related keratins, such as K16. The research highlighted the essential role of K17 in maintaining the structural integrity of initial hair and the survival of hair-producing cells. The study also suggested that clinical heterogeneity in conditions like pachyonychia congenita or steatocystoma multiplex could be due to cell type-specific, genetically determined compensation by related keratins.