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Several groups had previously reported that mutations to the binding site could make the virus switch its preference from bird to human cells.
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This fortuitous binding site could later prove to be a useful binding site for other low molecular mass partners.
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.
Presumably, a ligand-binding site could exist in the groove.
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.
First, although existent geometry-based methods provided considerable accurate prediction of binding site, improvement could be made by integrating other information, such as evolutionary conservation.
In the case of AuxRE/AuxRE-like composite elements, multiplication of weak sites into tandem clusters could make binding with ARF factors highly cooperative and strong.
According to the 'futility theorem' put forward by Wasserman and Sandelin (2004), a genome-wide scan with a typical PWM could incur in the order of 1000 false hits per functional binding site, which would make such an approach practically infeasible for accurate determination of binding sites.
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