The present study demonstrates that transcription factor interactions are i
mportant in regulating the murine fasl promoter following TCR-mediated acti
vation. We used DNase I-footprinting, EMSAs, and transient transfection ass
ays to identify the minimal TCR signal-responsive region within the fasl pr
omoter. This region contains the previously identified binding sites for NF
-kappa 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 prom
oter function in a fashion dependent on NF-kappa B binding, However, mutati
on 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.