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. Author manuscript; available in PMC: 2010 May 8.
Published in final edited form as: Cancer Lett. 2009 Jan 14;277(1):114–120. doi: 10.1016/j.canlet.2008.11.035

Fig. 1.

Fig. 1

Sequence analysis of the K-Ras gene in CT 26 cells and the effects of LY2109761 on TGF-β-induced Smad-dependent and -independent pathways. A, Sequence analyses of PCR product from exon-1 of K-Ras using mouse genomic DNA as template shows a G to A substitution in codon 12 (GGT to GAT) (indicated by arrow). B, Lysates from TGF-β treated CT26 cells were immunoprecipitated with anti-Smad2/Smad3 polyclonal antibodies followed by western blotting with anti-Smad4 antibody (top panel). The expression of Smad proteins was analyzed (bottom section). C, CT26 cells were treated with TGF-β1 (5 ng/ml), LY2109761 (10 μM), or both for 0.5, 1 and 2 hours. Cell lysates were analyzed by western blotting with anti-phospho-Smad2 and anti-Smad2 antibodies. D, CT26 cells were treated for 4, 12 and 24 hours as indicated, and cell lysates were analyzed by western blotting with antibodies against PAI-1, phospho-c-Jun, c-Jun, phospho-ERK and ERK. Each experiment was repeated 3 times.