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To test this, HLA-A*02 01 HLA-A*02 01efolded with a UV conditional ligand were moleculeside-refoldede by photolysis and the binding of the fluorescent peptide FLPSDC*FPSV withmonitored by fluorescence polarisation in the absence or presence of TAPBPR.
This fluorescence polarization/anisotropy increases as the binding of the fluorescent ligand to the desired protein increases.
The detection in our assay is based on the binding of the fluorescent dye SYBR Green, which binds all double stranded DNA molecules.
This was followed by the addition of a two-fold molar excess of protein and the binding of the fluorescent biotin was detected for 300 seconds as quenching of the fluorescence.
It was found that the binding of the fluorescent beads saturated when a 10-fold or higher molar ratio of biotin to antibody was used.
A key step in the initiation of the intrinsic apoptotic pathway is the oxidation of cardiolipin, which is assessed in this study by measuring the binding of the fluorescent compound NAO through flow cytometry.
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In addition, we observed that, starting from the first hour of infection, a fraction of cells undergoing mitochondrial membrane depolarization also displayed the caspase-3 activation, as assayed by the binding of the fluorescent-coupled DEVD inhibitor to the activated form of caspase-3 (FLICA caspase-3 (FAM-DEVD-FMK)).
We first studied the binding affinities of the fluorescent proteins toward the two AuNPs by fluorescence titration.
The binding affinities of the fluorescent granisetron probes for the human 5-HT3AR were determined by competition binding studies with [H]granisetron.
The change in the binding affinity of the fluorescent micelles toward the RCA-1 lectin immobilized column was monitored with time to estimate the chain exchange.
Furthermore, changes caused by antibiotics on the surface of the bacteria were demonstrated by a reduction in the number of binding sites of the fluorescent probe and an increase in the ANS dissociation constant.
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