These data, in conjunction with reported characterizations of the acetylcholine binding site, support a model of toxin activity in which a single solvent-accessible toxin side-chain anchors the complex, with supporting weak interactions determining both the efficacy and the subtype specificity of the inhibitory activity.
Our phylogenetic analysis of the LexA proteins and their binding sites supports such an argument.
While the matrix similarity allows the assessment of the structural quality of a binding site, the number of conserved binding sites supports the possibility that these binding sites might be functionally relevant (62).
In silico prediction of putative transcription factor binding sites supports the hypothesis that CGB1 and CGB2 gene products are expressed in, and may contribute to, implantation and placental development.
The identification of two variable lead scaffolds with differential binding sites supports the possibility of developing specific inhibitors of P. aeruginosa phospholipase D, PldA.
Glucose has many well-characterized binding sites, supported by a high number (> 400) of PDB structures in which it is co-crystalized with diverse proteins (representatives from > 200 protein clusters, with a 50% sequence identity threshold).
The presence of GlxR binding sites support the view of a hierarchical regulation of several prominent aspects of the C. variabile metabolism, including the utilization of γ-amino butyric acid, lipolysis, and β-oxidation.
Fifth, 39 of the 42 MFA peaks center on ORC1/CDC6 binding sites, supporting the proposed function of ORC1/CDC6 as an initiator protein.
Similar to the binding described above, substitutions to the complementary face of the 5-HT3B suBunit (B–) produce receptors with recovery rates more similar to those from 5-HT3A recontainingntaining only A+A− binding sites, supporting the hypothesis that the interaction of VUF10166 at an A+B− interface is responsible for the observed differences between the homomeric and heteromeric receptors.
Strikingly, 13 genes contained VDREs but no TCF/Lef consensus binding sites, supporting the concept that nuclear β-catenin can activate vitamin D/VDR target genes in the absence of TCF/Lef.
