Figure 4
Figure 4. An A1 promoter, lacking the NF-κB site, can still be activated by IgE receptor crosslinking or treatment with the calcium ionophore ionomycin. (A) Schematic view of the 2 vectors with luciferase as a reporter, containing upstream regions of A1. The −389 pA1 Luc does not contain the NF-κB binding site. (B) C57 cells transiently transfected with −1996 pA1 Luc or −389 pA1 Luc show a 3- to 5-fold increase in luciferase activity after IgE receptor crosslinking or treatment with ionomycin (1 μM). (C) The increased luciferase activity was abrogated by the addition of cyclosporin A. Data represent mean plus or minus SEM from 2 or 3 independent experiments.

An A1 promoter, lacking the NF-κB site, can still be activated by IgE receptor crosslinking or treatment with the calcium ionophore ionomycin. (A) Schematic view of the 2 vectors with luciferase as a reporter, containing upstream regions of A1. The −389 pA1 Luc does not contain the NF-κB binding site. (B) C57 cells transiently transfected with −1996 pA1 Luc or −389 pA1 Luc show a 3- to 5-fold increase in luciferase activity after IgE receptor crosslinking or treatment with ionomycin (1 μM). (C) The increased luciferase activity was abrogated by the addition of cyclosporin A. Data represent mean plus or minus SEM from 2 or 3 independent experiments.

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