FIG. 6.

Activation of P₆₇₀ by disruption of the hSkn–1a/YY1-binding sites. The nucleotide substitutions (see the legend to Fig. 3C) were introduced in sites 1 and 2 in mTATA/p670–Luc to generate plasmids lacking binding sites for hSkn–1a/YY1. HeLa cells were cotransfected with 0.2 μg of the plasmids with the mutations and 0.2 μg of pCMV4 or pCMV/Skn–1a. Luciferase activities of cell extracts were measured at 48 h after transfection. Results are presented as means ± standard deviations of three independent experiments.