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: The CaMK4-AKT-NF-κB pathway promotes KC pro-inflammatory phenotypes.The alternative text for this image may have been generated using AI.

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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