Key result
Mutation of the CRE/ATF-like site in the IL-1 beta gene upstream regulatory sequence resulted in a loss of approximately 75% of promoter activity in stimulated U937 and THP-1 cells.
Population
U937 and THP-1 monocytic cell lines
Comparison
Transfection with pIL1-CAT and treatment with… vs Uninduced cells or wild-type promoter sequences
Design
Preclinical
Authors
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Highlights CRE/ATF-like site for IL-1β control in monocytes; leaves open therapeutic implications for cardiovascular inflammation.
A CRE/ATF-like site is essential for the maximum induction of the IL-1 beta gene in stimulated U937 and THP-1 monocytic cells.
Gray et al. (1993) studied this question. Site-directed mutagenesis of the CRE/ATF-like site vs. Wild-type sequence was evaluated on Promoter activity. Mutation of the CRE/ATF-like site in the IL-1 beta gene upstream regulatory sequence resulted in a loss of approximately 75% of promoter activity in stimulated U937 and THP-1 cells.
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