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. Author manuscript; available in PMC: 2016 Apr 19.
Published in final edited form as: Sci Signal. 2016 Apr 5;9(422):ra34. doi: 10.1126/scisignal.aad5736

Fig. 1. mTOR activity is reduced by class I HDAC inhibition.

Fig. 1

(A) 3H-Leucine incorporation in NRVMs stimulated with PE, ET-1, IGF1, or 50% hypo-osmotic solution (HS) and exposed to the HDAC inhibitor apicidin (Api) (n=4). Con, control. (B) Western blot of mTOR downstream targets in NRVMs treated with HDAC inhibitors or rapamycin for 6h with quantification of S6 and 4EBP1 phosphorylation (n=6). p, phospho. (C) 3H-Leucine incorporation in NRVMs exposed to HDAC inhibitors and/or rapamycin (n=3–6). (D) Western blot for mTOR activity in NRVMs treated with PE, ET-1, IGF-1, or 50% HS and apicidin (n=3). (E) Western blot analysis of HDAC1, HDAC2 and HDAC3 knockdowns in NRVMs (n=3). (F) Total HDAC activity of NRVMs depleted of HDAC1, HDAC2 and/or HDAC3 (n=4). H, HDAC. (G) 3H-Leucine incorporation in NRVMs depleted of HDAC1, HDAC2 and/or HDAC3 and stimulated with PE (n=6). (H) Western blot and quantification of S6 phosphorylation in NRVMs depleted of HDAC1, HDAC2 and/or HDAC3 (n=3). Values are mean ± SEM, analyzed by one-way ANOVA followed by Tukey's test; * denotes p<0.05 sample compared to control (white bar); # denotes p<0.05 between groups marked; n= independent experiments.