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*
Department of Medicine, Arthritis Center, and
Department of Pathology, Boston University School of Medicine, Boston, MA 02118
l
The present study demonstrates that transcription factor
interactions are important in regulating the murine fasl
promoter following TCR-mediated activation. We used DNase
I-footprinting, EMSAs, and transient transfection assays to identify
the minimal TCR signal-responsive region within the fasl
promoter. This region contains the previously identified binding sites
for NF-
B and Egr and the AP-1 site identified in this study. We
found that TCR signaling induces AP-1 binding to this site and
regulates the fasl promoter function in a fashion
dependent on NF-B binding. However, mutation in the AP-1 site alone
did not show a significant effect on the promoter function. The data
suggest that the minimal promoter required at least two transcription
factors to function.
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