Fig. 8: The CaMK4-AKT-NF-κB pathway promotes KC pro-inflammatory phenotypes. | Nature Communications

Fig. 8: The CaMK4-AKT-NF-κB pathway promotes KC pro-inflammatory phenotypes.

From: Calcium/calmodulin-dependent protein kinase IV promotes imiquimod-induced psoriatic inflammation via macrophages and keratinocytes in mice

Fig. 8

HaCaT cells were transfected with siCAMK4 or scrambled control for 24 h. Then the cells were stimulated with recombinant human TNF (50 ng/ml) and IL-17A (50 ng/ml) for 24 h. The cells were harvested for analyses of apoptosis, cell cycle, and gene and protein levels. a Representative flow cytometry plots of HaCaT cell apoptosis. b The proportions of early and late apoptotic cells (n = 6 biologically independent samples). c Statistical analysis of G0/G1, S, and M phases of cell cycle (n = 4 biologically independent samples). d The expression of pro-inflammatory genes as determined by quantitative PCR (n = 3 biologically independent samples). e Co-IP assay of CaMK4 and AKT. f Western blot analysis of CaMK4, p-AKT, AKT, p-IKKα/β, IKKα, p-NF-κB p65, and NF-κB p65. The experiments in a–f were repeated three times with similar results. Data are shown as mean ± SD. For (a–d), two-sided unpaired Student’s t test. Source data are provided as a Source Data file.

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