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The cruzain inhibitory activity of some of these compounds was evaluated and a binding model was proposed.
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A microscopic binding model is proposed based on the studies of -1EF+2EF and +1EF-2EF that determine their microscopic binding constants (kI and kII for EF1 and EF2) and the studies of NCaBD that determine their overall binding constants, β1 and β2.
Based on the probing data, the architecture of the emitter site in the "non-binding" model was proposed.
We concluded that an intrinsic feature of the IFN-blocking antibodies was responsible for the observed "IFN-like" activation of EC; a model was proposed of antibody binding to surface Fc-receptors with sequestration of autocrine IFN and subsequent release to nearby IFN receptors, which would result in the observed "IFN-like" signal.
Hill equation, originated from the NICA model, was proposed to describe the binding of different species onto homogeneous substrates.
To explain this, a differential cooperativity model was proposed, in which there is self-cooperative binding of the repressor but not activator isoform of Ci.
A cancer stem cell model was proposed.
An Opportunities for Change Model was proposed.
Accordingly, the ABCDE model was proposed [ 12- 14].
A multiple protein or multifunctional receptor-ligand binding mechanism model is proposed as a way of visualizing the details and possible role of both the stacking and cleft type molecular recognition factors in the expression of biological activity.
A binding affinity based regulatory model is proposed to quantify the transcriptional regulatory network.
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CEO of Professional Science Editing for Scientists @ prosciediting.com