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. Author manuscript; available in PMC: 2010 May 1.
Published in final edited form as: Biochem Biophys Res Commun. 2009 Mar 13;382(2):424–429. doi: 10.1016/j.bbrc.2009.03.040

Figure 2. Effects of rapamycin on FGFR1-mediated downregulation of SM α-actin.

Figure 2

A. PAC1 stable cell lines were treated with DMSO or 10 nM rapamycin for 48 h and analyzed for mTOR kinase activity (Ser2448) by Western blot. The level of total mTOR served as loading control. B. Immunofluorescence staining of SM α-actin in PAC1 stable cell lines after treatment with DMSO or 10 nM rapamycin for 48 h. Images magnified 200× were acquired at similar exposure levels. C. PAC1 stable cell lines were treated with DMSO or 10 nM rapamycin for 48 h and analyzed for SM marker gene expression. β-tubulin served as loading control. D. PAC1 stable cells were transiently transfected with SM α-actin luciferase reporter and pRL-TK Renilla luciferase. After 24 h, cells were switched to 0.5% FBS with DMSO (black bars) or 10 nM rapamycin (gray bars) and incubated for an additional 48 h. Results were representative of three experiments and displayed as mean ± SD. * p < 0.05, as compared with the control. RLU, relative luciferase units. E. Quantification of the amount of newly synthesized SM α-actin in PAC1 stable cell lines treated with DMSO or 10 nM rapamycin for 48 h.