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In fact, it is difficult to envision how the transient state to the side of actin and that near the binding site could exhibit the same spatial extent in the probability density if the latter is highly localized (must be as the molecule is extended) and the former is a result of a completely free spherical search.
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Either visfatin or molecules that fit visfatin's binding site could help control the disease.
This fortuitous binding site could later prove to be a useful binding site for other low molecular mass partners.
Such interactions between elements around the binding sites could easily modulate affinity resulting in autoinhibition.
Identification of binding sites could facilitate design of DNA binding ligands for capture and detection of insulin and IGF-2.
The cross-linked binding sites could be adsorbed to wheat germ agglutinin and to anion exchange resins.
Presumably, a ligand-binding site could exist in the groove.
ADCs with diminished FcRn binding could exhibit shorter half-lives in vivo.
Interestingly, the WT-QR, which has mutations only in the NAD+ binding site, also exhibited increased specificity toward 3-HPA.
Products from a designed, sense/antisense gene for Class I and II ATP binding sites both exhibit appropriate catalytic activities.
The liver binding site exhibited an affinity 3.7-4.4-fold 3.7-4.4-fold 3.7-4.4-foldsmall intestine.
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CEO of Professional Science Editing for Scientists @ prosciediting.com