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This result is in line with our previous reports that binding was inhibited when surface epitopes were blocked by excess antibody applied before AFM was performed [19, 32].
FIV PPR SU-Fc bound strongly to 3201, but the binding was inhibited when pretreated with CXCR4 inhibitor AMD3100 (Figure 1A, right panel).
SA binding was inhibited when dGTP (+1 dNTP) was present (Figure 4B), and dGTP-dependent formation of heparin-stable complex was evident (Figure 4D).
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Furthermore, VCAM-MPIO binding to stimulated cells was inhibited when the VCAM-MPIO were pre-incubated with soluble decoy VCAM-1 (mouse recombinant Fc-VCAM-1) (Fig. 2A).
(b) SA binding to a biotin residue in the +2 position on the template was inhibited when +1 dNTPRTP/T complex was formed; whereas, binding to biotin in the +3 position was not affected.
The binding of guanine-rich DNA to the aptamer was inhibited when the aptamer captured 17β-estradiol.
Tzabcanin inhibited cell adhesion of both cell lines to immobilized fibronectin and vitronectin, and cell adhesion to immobilized tzabcanin was inhibited when cells were incubated with a cation chelator (EDTA), indicating that integrin tzabcanin binding is specific.
The synergic experiment showed that the VEGF binding was inhibited completely when 6a-P plus VEGF-Trap were present in binding media of HUVECs (Fig. 1B) and human liposarcoma cells (Supplemental Figure S1).
This binding was inhibited by increasing concentrations of unlabeled hPL (half-maximal concentrations, 2.2 and 3.4 nmol/L, respectively).
This binding was inhibited by anti-C3d.
This process contributes to the exciton linewidth broadening, while the dissociation channel of the excitons into the continuum state by 1-LO phonon absorption is inhibited when the exciton binding energy is larger than the phonon energy.
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