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. Author manuscript; available in PMC: 2009 Dec 8.
Published in final edited form as: Cancer Lett. 2008 Aug 12;272(1):91–101. doi: 10.1016/j.canlet.2008.06.032

Fig. 1.

Fig. 1

Effect of transfection of GSK3β mutant plasmids and LiCl treatment on the activation of GSK3β in A549 cells, as indicated by GSK3β phosphorylation on serine 9, i.e. p-GSK3β (ser9). A, Cells were transiently transfected with the constitutively active GSK3β mutant S9A-GSK3β (S9A) and dominant negative GSK3β mutant DN-GSK3β (DN) plasmids, as well as an empty vector control (vehicle), for 24 h. Whole cell protein was extracted and subjected to western blot analysis using a specific antibodies against GSK3β and p-GSK3β (ser9). β-actin served as control for equal protein loading. B, Western blot assay for expression of GSK3β and p-GSK3β (ser9) in A549 cells, following treatment with different concentration of LiCl as indicated for 24 h.