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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.
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An engineered PCNA gene with mutated E2F binding sites supports a low level of expression that can partially rescue the lethality of PCNA null mutants.
Furthermore, the composite nature of this binding site supports that FLAG-p7 adopts a hairpin fold in MeOH.
In addition, a fascinating hypothesis raises from the inspection of the proposed SHP structure: the presence of a potential unexpected ligand binding site, supported by recently available experimental data that may represent a breakthrough in the design and development of synthetic modulators of SHP functions.
The recently determined structure of the β2AR in an activated state revealed surprisingly subtle changes in the orthosteric binding site, supporting the idea that agonist binding and activation requires only modest conformational change in that region.
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.
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).
Our phylogenetic analysis of the LexA proteins and their binding sites supports such an argument.
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.
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).
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