Foxn1 Promotes Keratinocyte Differentiation by Regulating the Activity of Protein Kinase C

The study demonstrated that the transcription factor Foxn1 promoted the terminal differentiation of keratinocytes by regulating protein kinase C (PKC) activity. Foxn1 negatively affected PKC, as its absence led to increased levels of total, primed, and activated PKC, while its overproduction decreased phosphorylated PKC substrates. Applying PKC inhibitors to Foxn1-null keratinocytes normalized differentiation defects, indicating that Foxn1 acted as a brake on PKC signaling. This regulation allowed Foxn1 to control the timing of differentiation steps by modulating PKC activity.