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Role of activator protein-1 in TCR-mediated regulation of the murine fasl promoter
被引:25
|作者:
Matsui, K
Xiao, S
Fine, A
Ju, ST
机构:
[1] Boston Univ, Sch Med, Dept Pathol, Boston, MA 02118 USA
[2] Boston Univ, Arthrit Ctr, Dept Med, Boston, MA 02118 USA
关键词:
D O I:
10.4049/jimmunol.164.6.3002
中图分类号:
R392 [医学免疫学];
Q939.91 [免疫学];
学科分类号:
100102 ;
摘要:
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-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 promoter function in a fashion dependent on NF-kappa 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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页码:3002 / 3008
页数:7
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