Fig. 4
From: Keratin 6A promotes skin inflammation through JAK1-STAT3 activation in keratinocytes

KRT6A affects STAT3 activation and downstream cytokine expression in keratinocytes. A Immunoblotting of p-STAT3, STAT3, p-STAT1, STAT1, p-p65, P65, p-p38, P38, p-AKT, AKT, p-ERK or ERK in cell lysates from HaCaT cells infected with siKRT6A or Scr and stimulated with TNF-α for 2 h. Quantification of relative protein expression is shown in the right panel. B The STAT3 activation in KRT6A-overexpressed HaCaT cells. Quantification of relative protein expression is shown in the right panel. C Expression of STAT3 and pSTAT3 in cytoplasm or nucleus from HaCaT cells infected with siKRT6A or Scr and stimulated with TNF-α for 2 h. D Expression (left) and relative fluorescence intensity (right) of pSTAT3 in KRT6A-knockdown HaCaT cells treated with or without TNF-α for 2 h. E The mRNA levels of downstream cytokines in KRT6A-knockdown HaCaT cells. F Immunoblotting of p-STAT3 and STAT3 in skin lesions from LL37-induced mice treated with AAV-scr or Krt6a shRNA. Quantification of relative protein expression is shown in the right panel. All experiments were performed in 3 independent biological replicates. Data represents the mean ± SEM. *P < 0.05; **P < 0.01, ns for not significant. Two-tailed unpaired Student’s t-test (E) or 1-way ANOVA with Bonferroni’s post hoc test (A, B, D, F) was used