Fig. 5: STAT3 regulates wound healing gene expression in SPRR1B+ keratinocytes.
From: SPRR1B+ keratinocytes prime oral mucosa for rapid wound healing via STAT3 activation

a Heatmaps showing the transcriptional factors (TFs) which were differently expressed in each keratinocyte clusters. b The 10 TF genes with the highest scores in the Protein–Protein Interaction (PPI) network obtained by using the MCC algorithm of the CytoHubba plugin. c The predicted binding sites of STAT3 at the promoter region of SPRR1B gene. d Schematic of SPRR1B transcriptional start site (TSS) (red) and 0 to 500 bp upstream sequence. Design of PCR products for chromatin immunoprecipitation (ChIP) experiments (orange and red vertical lines) and predicted STAT3 binding sites (gray band) are indicated. e ChIP-PCR detection of STAT3 binding to the SPRR1B promoter region. f Western blot of STAT3, p-STAT3, JAK1, p-JAK1 and SPRR1B in HOK cells with JAK1/2 inhibitor ruxolitinib (Ruxo).