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The binding sites were defined by mapping the topographical arrangement of the phenyl rings, N-atoms and the electronegative atoms as described by Gund et al. [13].
To generate snapshots along the putative ligand path, three binding sites were defined within the channel of the crystal structure of Ops* (PDB entry 3CAP, Figure 4a).
Start and end coordinates of the binding sites were defined as the positions were the number of reads reached 50% of the peak height.
In the previous studies, protein-DNA binding sites were defined as those protein residues within a certain distance threshold to the DNA molecule bound to it.
For sites with known ligand binding, the binding sites were defined by protein residues, for which heavy atoms are within 6 Å of the ligand molecules.
127 "synergy genes" with NF-κB and STAT1 binding sites were defined by ≥2-fold Pol II binding within the 50-kb promoter region after hkL/IFN-I co-treatment compared with single treatment.
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Putative binding sites are defined by keeping a reduced set of ASPs separated by a minimum threshold of 8 Å. Pockets are ranked by the probe weights of their corresponding ASPs.
The primary ph4 for the σ binding sites was defined by mapping the topographic arrangements of the phenyl ring, the N-atom, and N lone pair vector; a point was placed 2.8 Å tetrahedrally from N atoms to represent an interaction between a protonated N atom and its binding site; dummy atoms were built 3.5 Å above and below a phenyl ring to represent hydrophobic binding to a receptor.
These binding sites are defined as the receptor regions within the radius of 10 Å centred on Met44 (opening A, 90° kink of the channel), Tyr268 (retinal binding pocket) and Ala269 (opening B).
Temporal activation of transcription factor binding sites is defined as the occupation of transcription factors on these sites over time in which causing the regulation mRNA expression of a particular gene.
The H3K27ac signal at co-localized single p63 binding sites was defined by the calculation of RPKM using a 4-kb window around the identified p63 ChIP-seq peak center from the H3K27ac ChIP-seq datasets of all four differentiation stages of HKC1.
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