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Effect of MPK38-mediated phosphorylation of Smad proteins on TGF-β-induced transcriptional activity. A–D, HepG2 cells were transfected with 0.2 μg of p3TP-Lux plasmid, increasing amounts of wild-type (WT), and kinase-dead (K40R) MPK38, and wild-type and mutant forms (S245A of Smad2, S204A of Smad3, S343A of Smad4, and T96A of Smad7) of Smad proteins (each 6 μg), as indicated, in the presence or absence of TGF-β1 (100 pm).
