Notes: CHO-K1 cells were transfected at ~80% confluency with four plasmids: (1) a CMV-driven vector expressing the wildtype or mutant human insulin receptor; (2) a pGL3-Basic-derived Vector containing five GAL4 binding sites upstream of the firefly luciferase reporter; (3) the pRL-CMV Control Vector; and (4) a fusion of the GAL4-binding domain and Elk-1 transcription factor. The Dual-Luciferase^® Reporter Assay System was used to confirm that specific mutations in the insulin receptor negate its ability to activate the Elk-1 transcription factor. (0896)

Notes: Vascular smooth muscle cells were transfected with a firefly luciferase reporter vector and pRL-SV40 as a control. Transfection efficiency was normalized to the Renilla luciferase activity as determined by the Dual-Luciferase^® Reporter Assay System. (0555)