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The dynamics of the switching and the biological properties of the surface were studied by observing the binding events between biotin and fluorescently labeled neutravidin.
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Lipid binding was measured by observing the change in the SPR angle as 150 µl of lipid analyte (various concentrations) in HBS-EP buffer flowed over the biosensor for 3 min at 50 µl/min.
The binding of cholesterol to P2 was monitored by observing the protein fluorescence quenching induced by stoichiometric amounts of ligand.
We first assessed the binding patterns of the three individual cell lines that were employed as CTC models, by observing their binding behaviors with each antibody using a flow chamber.
We investigated the commonality and specificity of transcription initiation factors in the RP gene family by observing transcription factor binding sites (Fig. 2).
Since this loop is located very close to the adenine of the substrate AMPCPP and contains one of the catalytically essential aspartic acid residues (Asp 99), the conformational flexibility observed by the binding of the bicarbonate ion and propagated via the movement of Arg 176 could influence the mechanism by which the bicarbonate ion exerts its allosteric regulatory role.
However, the binding abilities of these antibodies were 45 60% restored when this residue was replaced by tyrosine, a similar situation that had been observed in the binding studies.
Protein-based NMR assays detect ligand binding by observing changes in NMR nuclei in the target protein in response to test ligands.
It was observed that the binding of the inhibitor 2-aminoperimidine established interactions different from those introduced by the binding of the native ligand.
Phosphatidylserine externalization was assessed by observing at fluorescence microscopy the extent of streptavidin-fluorescein isothiocyanate (FITC) annexin-V binding.
Furthermore, we demonstrated that activation of the Wnt/β-catenin signaling pathway by LiCl and LEF-1 downregulation by using siRNA regulates MMP-9, 13, 14, ADAMTS-5, and COL10A1 expression, evidenced by the observed strong binding of LEF-1 to MMP-9, 13, 14, ADAMTS-5 and COL10A promoters.
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