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. 2014 Oct 7;9(10):e109811. doi: 10.1371/journal.pone.0109811

Figure 4. Treatment with 17-N-Allylamino-17demethoxygeldanamycin (17-AAG, an inhibitor of HSP90) resulted in nuclear localization of YAP/TAZ in immortalized corneal epithelial cells.

Figure 4

(A) Toxicity of 17-AAG to hTCEpi cells was observed at doses ≥50 nM. (B) Treatment with 45 nM of 17-AAG inhibited the protein expression of HSP90, TAZ and phospho-YAP (Ser172) in these cells without influencing the expression of total YAP. Blots are representative of data obtained from three individual experiments and graph demonstrating relative optical density are mean ± standard deviation from 3 experiments. (C) Reduction in cytoplasmic distribution accompanied by increased nuclear localization of YAP/TAZ was more apparent in cells treated with 45 nM 17-AAG (red channel for YAP/TAZ and blue channel for nucleus). Statistical comparisons were performed using one-way Kruskal-Wallis multiple comparison, ***p<0.001 compared with control (0 nM).