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Since many chemicals have been shown to interact with the AhR and influence transcription through the DRE, the presence of the mcsDRE in the pGL3 luciferase plasmid may inappropriately influence promoter and enhancer analysis.
SNPs that alter residues outside the -10 motif may also influence promoter activity.
Positions could be detected were the choice of nucleotides is likely to influence promoter strength.
Proteins that directly bind the promoter or indirectly influence promoter activity have been reviewed recently [ 3].
These same modifications can also influence promoter selectivity, thus directing p53 to different target genes [ 20, 21].
Consistently, the upstream truncation of the promoter fragment from position −85 to position −42 did not influence promoter activity.
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Another recent study revisited this phenomenon and showed that introns and splicing activity influence promoter-proximal chromatin profiles, Pol II occupancy, and overall transcriptional output [ 24].
This periodic structure includes the A + T-rich UP-element of bacterial promoters known before but was found to extend up to −100, indicating hitherto unknown constraints influencing promoter architecture and possibly also promoter function.
To determine whether E2 influences promoter usage, monocytes and macrophages were treated with E2 for 72 hrs and promoter usage was analyzed.
Finally, sSNPs might be causal through influencing promoter activity and the conformation and stability of pre-mRNAs[18], or changing the rate of protein folding[19].
Thus starting from a large pool of potential regulatory SNPs, we successfully identified a small fraction that actually influenced promoter activity.
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