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Using chromatin immunoprecipitation (ChIP) and primers designed to flank these YB-1 putative binding sites, we found evidence that YB-1 binds to the SOX2 promoter at two adjacent regions.
Among GR binding sites, we found that 46%% occur at enhancers having all three marks.
Despite the co-localization of AGO1 with CTCF and HP1α binding sites, we found a weak but independent binding motif for AGO1.
Although the computational sequence analysis of 2.2 kb upstream of the pre-miR-29b1 stem indicated four putative CEBP binding sites, we found that none of them was CEBPA responsive in luciferase assays (data not shown).
Moreover, when we broadly searched PlasmoDBv10.0 transcripts for human microRNA binding sites, we found thousands of significant hits and that 61 transcripts harbored at least 100 predicted binding sites for a given human microRNA (p-value < 0.05) [Additional file 32].
By mapping the genomic binding sites, we found that both TBP and Pol II display greater than 63% occupancy at transcriptional start sites (TSS) of highly expressed genes in both undifferentiated C3H10T1/2 cells and adipocytes, consistent with their roles in mediating global and general transcription functions.
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Assessing the content of the established consensus sequence for STAT1 binding sites, we find that the usage of "negative control" ChIP-seq data fails to provide substantial advantages.
Based on over-representation analysis of their binding sites we find that the expression pattern for the genes of these six transcription factors correlate nicely with the time profiles of their putative target gene clusters.
When several known factor Xa inhibitors were overlaid within the protein binding site, we found that they all bind within the groove formed by the S1 and S4 sub-pocket of fXa (Figure 10B).
Site1, the binding site we found by DS2.1 automatically searching, can cover the structural domain included by endogenous ligand.
Interestingly, using a reporter system containing Nanog response element (binding site), we found that Li significantly enhanced the expression of reporter in HEK293T cells co-expressed with Nanog.
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