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This analysis selects transcription factors whose binding sites are enriched in ChIP-enriched regions compared to background promoters (see Methods).
Thus, Insm1, Neurod1 and Foxa2 frequently bind in close proximity in chromatin of pancreatic β-cells, and high affinity binding sites are enriched in sites co-occupied by all three factors.
Nucleosome positioning at distinct subsets of promoters additionally requires the essential Myb family proteins Abf1 and Reb1, whose binding sites are enriched in NFRs.
This analysis enables selecting transcription factors whose binding sites are enriched in ChIP-selected regions compared to background promoters.
Down-regulation of Dam during stationary phase correlates with the activity of TFs whose binding sites are enriched for GATC sites.
We have also identified AP-1 and C/EBP as collaborating transcription factors, whose binding sites are enriched in ChIP-seq-derived STAT1 binding regions.
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As expected, AR binding sites were enriched for AR motifs, as well as for its pioneer factor FOXA1 (Fig 3H, Appendix Fig S7, Table EV3).
Additionally, AR binding sites were enriched with sequence motifs recognized by the ABDB (Abdominal-B type homeodomain transcription factors) family (Additional file 3: Table S3), suggesting potential combinatorial control between androgen receptor and homeobox genes.
Many transcription factor binding sites were enriched, including motifs binding the oncoprotein MYC (Table S3).
Therefore, we sought TFs downstream from EGF whose binding sites were enriched in promoters of upregulated tumor genes.
Several transcription factor binding sites were enriched in these differentially regulated target genes, including CCAAT-displacement protein (CDP).
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