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These results suggest that the activation and binding model could be different for each TLRs because their ligands are fundamentally different.
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Note that once a pair of a kinase and an inhibitor is classified as binding, a regression model could be applied subsequently to predict the quantity of the binding affinity.
The predicted binding affinities of the antagonists to CCR5 correlate well with the antagonist activities, and the interaction model could be used to explain many mutagenesis results.
Determine how the model could be improved.
Three-dimensional models could be equally misleading.
Nonlinear protein-binding models could not be identified based on the available data and were visually not observable.
As multiple PRD residues could simultaneously interact with a peptide residue and multiple peptide residues could simultaneously interact with a PRD residue [ 71], binding specificity could be more accurately modeled by considering covariation signals between residue groups.
Integrated heats from all the binding reactions could be fitted well with a single-site binding model.
Thus, while one can propose a simplistic model for how NikR binding to DNA could be regulated by nickel, this model fails when one considers the features needed for efficient binding site searching, perhaps explaining the need for a more complex mechanism of action.
In fact, after modeling Lac2 with 1ZPU (Fet3p) as template, no iron binding site could be observed (data not shown).
A characteristic binding motif could be deduced.
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Justyna Jupowicz-Kozak
CEO of Professional Science Editing for Scientists @ prosciediting.com