Figure 3.

Sema3e was a direct transcriptional target of RORα. A) Luciferase reporters with native (WT/Sema3e) or mutated RORα (MUT/Sema3e) binding sites in Sema3e promoter were cloned and cotransfected with varying amounts of RORα–expressing vector into HEK293T cells. RE, responsive element. B) Cotransfection of RORα–expressing vector dose-dependently suppressed WT/Sema3e luciferase expression in pGL2 vector, reflecting the transcriptional activity of WT/Sema3e (covering residues −634 to −638 bp). Luciferase activity from mutant constructs of MUT/Sema3e did not respond to RORα cotransfection. C) SR1001 treatment dose-dependently promoted WT/Sema3e promoter–driven luciferase reporter activity but did not promote MUT/Sema3e RORE reporter constructs (n = 6/group). Data are presented as means ± sem. N.s., no significance. *P < 0.05, **P < 0.01.