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. 2015 Aug 20;19(5):467–472. doi: 10.4196/kjpp.2015.19.5.467

Fig. 5. Trichostatin A (TSA) inhibited angiotensin II-induced p66shc phosphorylation in HEK293T cells, ectopically expressing angiotensin II receptor type 1. (A) Fluorescence images of EGFP-tagged angiotensin II receptor type 1 or type 2 (×400 magnification). HEK293T cells were transfected with EGFP (upper), EGFP-tagged angiotensin II receptor type 1 (middle) or type 2 (lower). The plasma membrane was stained using CellMask Deep Red solution. (B) Cells expressing angiotensin II receptor type 1 were pretreated with either DMSO (control) or the indicated concentrations of TSA for 30 min. The cells were then either left untreated (DMSO), treated with TSA alone (controls), or exposed to 100 nM angiotensin II in the presence of TSA for 30 min. Western blotting was performed for phospho-p66shc and Shc. Bars represent the mean phospho-p66shc/p66shc levels±S.E.M. (n=3). **p<0.01 (vs. control), *p<0.05 (vs. control), #p<0.01 (vs. only angiotensin II-treated cells).

Fig. 5