Nevertheless, based on the absolute conservation of residues important for cap binding and the strong FR results, we predict that L529 is a translation initiation factor and hypothesize that it may participate in cap-dependent translation.
Based on the identification of the same binding motifs, we predicted that a common regulatory mechanism of miR-433 and miR-127 expression may exist among different mammalian species.
Since different binding affinities were noted for CpG and non CpG DNA upon binding to TLR9, we predicted that CpG-TLR9 and non CpG-TLR9 bound complex might have different intracellular mobilities.
Given the peculiar conservation of the weak Rap1 binding site at HMR-E, we predicted that the genome-wide consensus binding site for Rap1 would not silence the HMR - a1 gene as effectively as the native Rap1 binding site.
We predicted that binding at test would be augmented for actions that were previously trained with entirely novel, and therefore surprising, outcomes.
Using molecular simulations, we predicted that the binding interface between DARPin off7 and its ligand (maltose binding protein; MBP) is characterized by a hot-spot motif in which binding energy is largely concentrated on a few amino acids.
Since variant RcsB proteins lost DNA-binding activity (Fig. 4C), we predicted that variant RcsB proteins would not repress flhDC expression in vivo.
For rs2431697 (miR-146a), we predicted that the binding of transcriptional repressor protein YY1 (YY1 gene) may be disrupted in the corresponding variant region of minor allele G. Importantly, we observed a very significant binding affinity change for androgen receptor (NR3C4) in the rs2732547 (CD44) located region for a different allele.
Since Val923 does not alter dsRNA binding [5], we predict that the amino acid substitution reduces the efficiency of IFIH1 interactions, possibly with interferon-beta promoter stimulator protein-1 (MAVS, mitochondrial antiviral signaling protein, also known as IPS-1, VISA and Cardif) during anti-viral signaling [14].
We predicted that these DNA-binding sites should be found in the promoter region of genes expressed in the endoderm, where Hox and TALE products are present together.
