FIG. 5.

MAPK potentiates c-fos–junD activation of the A-TRE. (A) HeLa cells maintained in 0.5% fetal calf serum were transfected with an A-TRE plasmid (3 μg) and expression vectors encoding p44/ERK-1 (2 μg) or c-fos (cf)–junD (jD) (2 μg in total), or both together. The ERKDN mutant is a dominant negative kinase-deficient ERK-1. The effect of cotransfection of a constitutively activated PKC (β isozyme) is also shown. (B) The ability of MAPK to potentiate junD-fos (f) induction of the A-TRE was also determined on c-fos C-terminal mutants. HeLa cells were transfected with a 3× A-TRE plasmid (3 μg), ERK-1 plasmid (2 μg), and junD/c-fos (or mutant) plasmids (2 μg). sA, sB, and sC, serA, serB, and serC. Except for panel C, where the results from a representative experiment carried out in duplicate are shown, the data presented are the means ± standard deviations of four to six independent determinations. (C) The effect of MAPK on the A-TRE was also tested in ventricular cardiocytes by cotransfection of 1× A-TRE (3 μg) with junD–c-fos (2 μg), in the absence or presence of MAPK vectors (2 μg).