Sentence examples for binding assay with an from inspiring English sources

We used a filtration-based binding assay with an SRIF-14 based competing hot ligand (125I-[Tyr11]-SRIF14), whereportsher reports used an autoradiography approach and the SRIF-28 analog: 125I-[Leu8, DTyr25]-somatostatin-28atin-28 (Fani et al. 2012b).

We also estimated the amount of 8-oxoG using a fluorescence-based binding assay with an avidin-conjugated TRITC reagent [ 25].

DV1 has been shown to compete more efficiently with [I]SDF-1α in the CXCR4 binding assay with an IC50 of 13 nM than the nonmodified V1 peptide (IC50 = 218 nM).

c Lindmo binding assay with a constant 111In-DOTA-belatacept concentration of 0.5 nM.

Furthermore, we outline the design of a binding assay with a tethered bilayer and the procedure of the artificial membrane system built-up is delineated.

We examined AR binding affinities of our compounds in a competitive binding assay with a radiolabeled high affinity AR ligand, 3H-mibolerone, and also measured their abilities to stimulate AR-mediated transcriptional activation in a cotransfection assay.

Equilibrium fluorescence anisotropy binding assays with a fluorescein (FAM -labeled A10-RNA were used to monitor FAM -labeled the closed state with increasing concentrations of NDP-BeFx (N = A, C, G, or U; Figure 2B).

Peptides 5, 6, 9′, and 10′ were used in B16F10 melanoma cell competitive binding assays with a standard radiolabeled MC1R binding peptide, I- Tyr -NDP, to confI- Tyr -NDPe modI- Tyr -NDPmade to the peptides through linker attaconfirmand methatcomplexathen did not abrogate their affinity for the modifications

The in vitro binding data showed that the (S -isomer of II waS -isomerin the bradykinin B2 receptof-bIIding assay wash a Ki of 33 nM.

Using a highly sensitive ligand-binding assay with a Gaussia princeps luciferase fusion protein of the TNFR1-specific TNF mutant 32W/86T, we were able to detect significant TNFR1 expression in five additional cell lines (U266, OPM2, KMS-11, INA6 and JJN3) while even with this assay there was no evidence for TNFR1 expression in AMO1 and L363.

The HLA-A24 binding ability was then assessed using a HLA-A24 binding assay with SL8C peptide as a negative control and Survivin-2B_80 9 Survivin-2B_80 9ontrol.