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A paucity of binding sites has also been observed in other OCT4 ChIP-on-Chip experiments [3], [14] where less than 5% of target genes had the OCT4 binding motif.
Significant similarity in FFRP binding sites has also been observed between LrpB and LysM in S. solfataricus [ 24].
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IgF binding sites have also been reported on trout MR [70].
An unexpectedly large number of binding sites have also been observed for several transcription factors in Drosophila, suggesting this is a general feature of these factors [28], [29], [30].
Mutations in HNF4α binding sites have also been directly linked to human diseases, including hemophilia and MODY3 [ 31, 32].
CTCF binding sites have also been shown to be under positive selection in several Drosophila species [ 18].
Heme binding sites have also similarly been designed into native α-helical bundle proteins that do not have native heme binding sites.
More rarely, peptides with substitutions at MHC binding sites have also shown interesting properties as APL 4, 5 such as stimulation of partial agonist responses 5.
Relaxin binding sites have also been detected in blood vessels from humans, as well as in cells and tissues from the human heart [ 38].
Most target genes contain one or more binding sites for TCF/LEF proteins, which prefer a common core DNA binding site with the consensus CTTTGWW, although other divergent binding sites have also been characterized (Cadigan 2012).
We also examined whether there was an overlap between intergenic CSSs and the binding sites for C-MYC and SUZ12, factors for which binding sites have also been experimentally mapped [ 26, 27].
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