To test this hypothesis, we compared the binding sites of a mutant KAP1 with no RBCC domain (mt KAP1) versus the binding sites of wild-type KAP1 (wt KAP1) on HEK293 cells (see Materials and Methods section).
The interaction of these hybrids was also investigated by the molecular docking studies in the binding site of wild type Pf-DHFR-TS and quadruple mutant Pf-DHFR-TS (Table 33, Fig. 9) [44].
We postulated that by using an inactive mutant CTB protein as the scaffold, once modified with carbohydrates, the resulting pentavalent ligand should provide a precise fit of the ligand groups with the spacing and configuration of binding sites on wild-type CTB.
Masitinib was docked into the ATP-binding site of wild-type KIT and ABL using the coordinates of human KIT and ABL in the inactive conformation.
After manual adjustment, the final monomer structure was refined with one full occupancy molecule of DRV oriented approximately perpendicular to DRV in the typical inhibitor-binding site of wild-type PR or most mutants, as indicated by the clear electron density map.
The contribution of the + 3 subsite to the substrate specificity of BsXynA was established more in detail by mapping the enzyme binding site of the wild type xylanase and mutant Y88A with labelled xylo-oligosaccharides.
However, because of its small size, 5HFA resides loosely in the binding site of the wild type enzyme (Additional file 7C), which explains its low affinity and reduced turnover of 5HFA compared with tricetin.
To this end we determined the binding sites of FLI1 and SCL/TAL1 in wild-type c-kit+/CD41+/Tie2− progenitor cells (c-kit+ cells) and obtained 7735 and 8205 peaks, respectively and 1371 joint peaks.
Color-coded letters indicate the locations of the wild type binding sites of transcription factors in intron enhancer (IE), while the dashed colored lines represent deletions of that particular site.
As shown in Figure 3D, cells transfected with the −298/22κB wt construct, which had both wild-type binding sites of RELA/p50 and STAT5, had the highest reporter activity, followed by −298/22κB mut and −207/+22 constructs, which contained only one intact STAT5 binding site.
To test whether Egr2 is post-transcriptionally inhibited by miR-17-92 miR-17-92 miR-17-92of murine Egr2 3′UTR containing two wild-type binding sites of miR-17-92 or their mutants were subcloned into the pGL3-Promoter vector, downstream of the firefly luciferase gene.
