DLX3 is a homeodomain transcription factor involved in epidermal and hair follicle differentiation. Epidermal specific deletion of DLX3 leads to IL17 related inflammation.;	However, the downstream signals from DLX3-deficient keratinocytes that initiates IL17 associated inflammation is not well-characterized. Therefore we performed acute Dlx3 deletion to identify the initial molecular changes causing the skin inflammatory reponse and tried to rescue the immune phenotype by STAT3 inhibitor treatment (Cryptotanshinone).;	In this study, we compared the epidermal and dermal transcriptome from Dlx3 wild-type (WT) and K14CreERT;DLX3 fl/fl (icKO). SOURCE: Maria,Irene,Morasso (morassom@mail.nih.gov) - Laboratory of Skin Biology NIAMS NIH

Pluto Bioinformatics

GSE104022: Molecular consequences of Dlx3 deletion by tamoxifen inducible K14 Cre in adult mouse epidermis (P42-P46) as determined by RNASeq analysis