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. 2008 Nov 7;283(45):31183–31196. doi: 10.1074/jbc.M801606200

FIGURE 5.

FIGURE 5.

Identification of the GC-responsive region in the human CALD1 promoter. A, reporter assay was performed with the human fibroblast-type (-964 to +101) and HeLa-type (-1908 to +207) CALD1 promoters in A549 cells co-transfected with the luciferase reporter plasmid and pGL3β-gal plasmid. The cells were incubated with vehicle or 1 μm DEX for 24 h. The luciferase activities were normalized to the β-galactosidase activity (mean ± S.D., ***, p < 0.001). B, effect of GR or MR antagonists on the fibroblast-type CALD1 promoter activity (mean ± S.D., **, p < 0.01, ***, p < 0.001). C, effect of GR or SRF depletion on the fibroblast-type CALD1 promoter activity (mean ± S.D., **, p < 0.01; ***, p < 0.001). D, luciferase activities in A549 cells co-transfected with reporter plasmids and the pCS2+GRΔC-cFLAG plasmid were measured after a 24 h incubation (mean ± S.D., **, p < 0.01). E, schematic diagram of deletion and mutation constructs of the CArG element or GRE-like sequences in the human fibroblast-type CALD1 promoter. F, GRΔC-responsiveness of the promoter activities of a series of reporter constructs (mean ± S.D., **, p < 0.01; ***, p < 0.001; n.s., not significant).