Making the reasonable assumption of a synergistic effect for the mutations [60], a triple Y72N/Y124Q/Y337A mutation encompassing both the peripheral and choline-binding sites could increase Ki by over two orders of magnitude.
It was thus hypothesized that these putative GATA binding sites could contribute to the increased Rluc gene activities observed.
Combinative use of more than one computational algorithm in the prediction of miRNA binding sites could decrease the false positive rate, but it might increase the false negtive rate because the overlap between computational algorithms is not very good.
Alteration of one or more of these transcription factor binding sites could reduce the levels of IκBα expression, increase NK-κB activity and contribute to HBV-induced hepatocarcinogenesis.
For example, new transcription factor binding sites could be created from background sequence through successive adaptive fixations that increase binding site strength; this would lead to an increase in S, and therefore ΔS would be greater than zero on average.
Identification of binding sites could facilitate design of DNA binding ligands for capture and detection of insulin and IGF-2.
For this kind of bound structures, binding sites could not be computed directly based on their ligands.
Neither cytotoxicity nor the competition between TCC and testosterone for binding sites could be observed in their studies.
Mutagenesis of the predicted binding sites could show if transcription factors are involved in this function.
For example, a transcriptional suppressor protein that competes with a transcriptional activator for the same binding site could result in decreased activation through increased methylation [13].
