Role of Activator Protein-1 in TCR-Mediated Regulation of the Murine fasl Promoter
Author(s) -
Ken Matsui,
Sheng Xiao,
Alan Fine,
ShyrTe Ju
Publication year - 2000
Publication title -
the journal of immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.737
H-Index - 372
eISSN - 1550-6606
pISSN - 0022-1767
DOI - 10.4049/jimmunol.164.6.3002
Subject(s) - activator (genetics) , microbiology and biotechnology , promoter , transcription factor , fas ligand , biology , t cell receptor , footprinting , transcription (linguistics) , transfection , binding site , gene , t cell , genetics , gene expression , apoptosis , programmed cell death , linguistics , philosophy , immune system
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-kappaB 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-kappaB 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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