As we find no indication that genes underlying intQTL directly bind to these regions as transcriptional regulators, we speculate that the interaction is downstream of rQTL function, potentially by protein protein interactions between the products of rQTL and intQTL genes.
These signals bind to transcription regulators, and induce the expression of virulence genes such as exotoxins and proteases.
Alternatively, these GLS elements may bind to other transcriptional regulators.
Two independent groups individually found CIP2A directly bind to cell-cycle regulators including polo-like kinase (PlK1) and never in mitosis gene A-related kinase 2 (NEK2) [ 19, 20].
To study, whether or not the transcriptional regulator directly binds to these target genes, we performed motif searching that lead to the identification of potential SrbA binding sites in the promoters of the predicted target genes.
Next, derived oligosaccharides are transported into cell, and these or other metabolites bind to a transcriptional regulator.
This impairs ability of p53 to bind to its negative regulator, MDM2 [ 35].
Other RNA regulators bind to proteins and regulate their function, whereas the largest group of small RNAs (sRNAs), act by base pairing with target RNAs.
They were bound to influence regulators, particularly in areas where they had greater expertise, a phenomenon known as "regulatory capture".
Another class of molecules called coregulators binds to regulators and affects transcription by either stabilizing or destabilizing interactions between regulators and the Basal-transcription machinery.
