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An antisense transcript named FAST-1 (FXN Antisense Transcript – 1), whose sequence overlaps with the CTCF binding site, has also been discovered.
In addition, the alteration at position 150 (138 in H3) from Ala to Ser, which may affect the conformation of residues lining the receptor binding site, has also been linked to changes in receptor specificity in H1 viruses [38].
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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].
In addition, a low-affinity RACK1-binding site has also been located in the PDE4D5 catalytic domain [ 11].
Although, much of this process as we understand it is due to the hydrolysis of ATP at the N-terminal domains of Hsp90, a C-terminal ATP-binding site has also been reported [67 71].
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.
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