| Experiment Id | GSE117375 | Name | Gene expression in Krt16 null paw lesions relative to WT paw skin |
| Experiment Type | transcription profiling by array | Study Type | WT vs. Mutant |
| Source | GEO | Curation Date | 2022-11-16 |
| description | The type I intermediate filament keratin 16 (Krt16 gene; K16 protein) is constitutively expressed in ectoderm-derived appendages and volar palmar/plantar epidermis, and is otherwise inducibly expressed in non-volar epidermis when skin epithelia are under stress. Mutations at the (human) KRT16 locus can cause pachyonychia congenita (PC) and focal non-epidermolytic palmoplantar keratoderma (PPK), which each entail painful calluses on palmar and/or plantar skin. Krt16 null mice develop footpad lesions that mimic several aspects of PC-associated PPK and FNEPPK, including hypoactive Keap1-Nrf2 signaling and elevated expression of skin barrier homeostasis genes and Danger Associated Molecular Patterns (DAMPs). This provides a unique opportunity to understand the intricacies of PPK and devise effective therapies (see Lessard and Coulombe, J. Invest. Dermatol. 2012; Lessard et al. PNAS (USA) 2013; Kerns et al. J. Clin. Invest. 2016; Kerns et al., J. Invest. Dermatol. 2018; Zieman and Coulombe Exp. Dermatol. 2018). Here, we report on insight gained from a genome-wide analysis of gene expression in PPK-like lesions of Krt16 null mice. In this dataset, we include expression data obtained from Krt16 null paw skin lesions and WT littermate controls (C57Bl/6 strain background) at two months of age. Paw skin was dissected from murine forepaws of Krt16 null and Krt16 WT littermates (C57Bl/6 strain background). A total of 8 mice were used, 4 Krt16 null (2 male, 2 female) and 4 Krt16 WT (2 male, 2 female). Mice were aged to two months before RNA isolation. |
