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. Author manuscript; available in PMC: 2013 Jul 31.

Published in final edited form as: Cell Oncol (Dordr). 2012 Jan 31;35(2):95–110. doi: 10.1007/s13402-011-0068-y

Fig. 4 — Effects of uPAR on ERK and RhoA in H460 cells. A. ERK activation was determined in quiescent, serum-deprived cells incubated with 10 nM of the indicated agonist or for 15 min Following treatment, cells were rinsed with PBS and lysed in Laemmli sample buffer. A total of 20 μg of each sample was resolved on a 10% sodium dodecyl sulfate–polyacrylamide gel electrophoresis and total ERK and phosphorylation state of ERK was determined by immunoanalysis. Data are representative of three separate experiments. B. (Top Panel) GTP bound RhoA was determined by affinity pulldown performed with GST-RBD following agonist treatment. Samples were blotted with an antibody against RhoA. Blot is representative of four blots. The normalized relative density of each blot was averaged (Lower Panel).

Fig. 4 — Effects of uPAR on ERK and RhoA in H460 cells. A. ERK activation was determined in quiescent, serum-deprived cells incubated with 10 nM of the indicated agonist or for 15 min Following treatment, cells were rinsed with PBS and lysed in Laemmli sample buffer. A total of 20 μg of each sample was resolved on a 10% sodium dodecyl sulfate–polyacrylamide gel electrophoresis and total ERK and phosphorylation state of ERK was determined by immunoanalysis. Data are representative of three separate experiments. B. (Top Panel) GTP bound RhoA was determined by affinity pulldown performed with GST-RBD following agonist treatment. Samples were blotted with an antibody against RhoA. Blot is representative of four blots. The normalized relative density of each blot was averaged (Lower Panel).