Skip to main content
. 2004 Feb;24(3):1081–1095. doi: 10.1128/MCB.24.3.1081-1095.2004

FIG. 6.

FIG. 6.

FHL2 inhibits ERK-mediated transcriptional activation. (A) A Gal4-dependent luciferase reporter construct (1.0 μg) was cotransfected into cardiomyocytes with expression vectors encoding Gal4DBD-ELK-1 fusion (0.25 μg), activated MEK1 (0.25 μg), and/or FHL2 (0.1, 0.25, or 0.5 μg). (Bottom) Control Western blots were performed for protein levels of MEK1, FHL2, and Gal4ELK-1 from the aligned transfection reactions. (B) A GATA site-dependent luciferase reporter construct (1.0 μg) was cotransfected into cardiomyocytes with expression vectors encoding activated MEK1 (0.25 μg) and/or FHL2. (C) An ANF promoter (luciferase) construct (1.0 μg) was cotransfected in cardiomyocytes with expression vectors encoding activated MEK1 (0.25 μg) and/or FHL2. (D) Cotransfection experiment with the Gal4-luciferase reporter (1 μg) and a construct encoding Gal4cJun and/or FHL2 (0.25 μg) at baseline or after serum stimulation in cardiomyocytes. (E) Cotransfection experiment with the Gal4-luciferase reporter and constructs encoding Gal4DBD-ELK-1 (0.25 μg), MEK1 (0.25 μg), RhoA-V14 (0.25 μg), and FHL2 (0.50 μg). (F) Cotransfection experiments with a MEF2-dependent luciferase reporter construct (1.0 μg) and expression vectors encoding ERK5 (0.25 μg), MEK5 (0.25 μg), and FHL2 (0.5 μg). All data in each panel are expressed as relative light units (RLUs) per microgram of protein (n = 3 independent experiments). +, present; −, absent.