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. 2017 Mar 31;13(6):4238–4244. doi: 10.3892/ol.2017.5962

Figure 4.

Figure 4.

Role of p300 in Akt1 acetylation and phosphorylation in nasopharyngeal carcinoma cells following exposure to IL-17A. C666-1 cells were transfected with p300 shRNA or control shRNA for 48 h prior to IL-17A stimulation. Co-immunoprecipitation and western blot analysis were further used to detect Akt1 acetylation and phosphorylation at 30 min following IL-17A stimulation. The results showed that p300 shRNA suppressed Akt1 acetylation and phosphorylation in C666-1 cells following exposure to IL-17A compared to the control shRNA treatment. **P<0.01 vs. control shRNA+IL-17A group. The data are from one experiment, and are representative of three independent experiments. Results are presented as the mean ± standard deviation (n=3 in each group). Representative western blot photographs were produced. IL-17A, interleukin-17A; IgG, immunoglobulin G; Ack, acelytated; Akt1, AKT serine/threonine kinase 1; p, phosphorylated; t, total; iso, isotype; IP, immunoprecipitation; p300, E1A binding protein p300; sh, short hairpin.