Fig. 2.
Fig. 2. The IL-4 receptor signaling pathway is intact in Jurkat T cells. (A) The luciferase reporter construct C/EBP-N4 luc (see text) was transiently transfected into Jurkat cells together with a control (Empty) or Stat6 expression vector. Cells were then stimulated without (□) or with (▪) IL-4 (50 ng/mL) for 18 hours before assays for reporter gene expression. In the absence of either cotransfected Stat6 or IL-4 stimulation, C/EBP-N4 luc is not active in Jurkat cells, but it is highly inducible by IL-4 in cells expressing Stat6. (B) Consistent with the known expression of Stat6 by Hep G2 cells,21C/EBP-N4 luc was induced by IL-4 in these cells, but its activity was further increased by overexpressing Stat6 (note the different scales). Results are the mean ± SEM of two (B) or three (A) independent experiments.

The IL-4 receptor signaling pathway is intact in Jurkat T cells. (A) The luciferase reporter construct C/EBP-N4 luc (see text) was transiently transfected into Jurkat cells together with a control (Empty) or Stat6 expression vector. Cells were then stimulated without (□) or with (▪) IL-4 (50 ng/mL) for 18 hours before assays for reporter gene expression. In the absence of either cotransfected Stat6 or IL-4 stimulation, C/EBP-N4 luc is not active in Jurkat cells, but it is highly inducible by IL-4 in cells expressing Stat6. (B) Consistent with the known expression of Stat6 by Hep G2 cells,21C/EBP-N4 luc was induced by IL-4 in these cells, but its activity was further increased by overexpressing Stat6 (note the different scales). Results are the mean ± SEM of two (B) or three (A) independent experiments.

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