Figure 2
Figure 2. ETS, CRE, and EGR binding sites contribute to basal expression of the VEGFR1 promoter in primary human endothelial cells. (A) Wild-type (WT) and mutant cis-regulatory sequences used in transfections and Hprt-targeted mice. The wild-type DNA sequence is shown on top (50-bp per line) with each of the ETS, CRE, and EGR binding sites individually colored, and the 5′ untranslated region underlined. The mutated sequences are shown underneath, underlined in parentheses. (B) WT or mutant VEGFR1 promoters were coupled to luciferase in PGL3 and the resulting plasmids were transiently transfected into HUVECs, HCAECs, or HPAECs. The results show the means and SDs of luciferase light units (relative to untreated cells) obtained in triplicate from at least 3 independent experiments. + indicates 0.1; **P < .01; ***P < .001.

ETS, CRE, and EGR binding sites contribute to basal expression of the VEGFR1 promoter in primary human endothelial cells. (A) Wild-type (WT) and mutant cis-regulatory sequences used in transfections and Hprt-targeted mice. The wild-type DNA sequence is shown on top (50-bp per line) with each of the ETS, CRE, and EGR binding sites individually colored, and the 5′ untranslated region underlined. The mutated sequences are shown underneath, underlined in parentheses. (B) WT or mutant VEGFR1 promoters were coupled to luciferase in PGL3 and the resulting plasmids were transiently transfected into HUVECs, HCAECs, or HPAECs. The results show the means and SDs of luciferase light units (relative to untreated cells) obtained in triplicate from at least 3 independent experiments. + indicates 0.1; **P < .01; ***P < .001.

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