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1 Ki compared with WT RGS2 in a flow cytometry competition binding assay).
2 independently our results with a minicircle competition binding assay.
3 -347, Lys-351, and Lys-414 was verified by a competition binding assay.
4 ed and validated a fluorescence polarization competition binding assay.
5 oluble Lf receptor activity as determined by competition binding assay.
6 d for their capacity to bind protein using a competition binding assay.
7 ity of LY2795050 was measured in radioligand competition binding assays.
8 (hD3) receptor (Ki = 1-5 nM) as measured in competition binding assays.
9 as observed by coprecipitation, overlay, and competition binding assays.
10 higher than their respective Ki values from competition binding assays.
11 sing ELISA, immunohistochemical studies, and competition binding assays.
12 er of potency comparable to that observed in competition binding assays.
14 ma (PPARgamma), we identified GW9662 using a competition binding assay against the human ligand bindi
15 employed in an automated fluorescence-based competition binding assay, allowing the pKi values of se
16 Evolution of pRNA aptamers was followed by a competition binding assay and nucleotide sequencing, and
17 to GPIIb/IIIa receptors was investigated in competition binding assays and autoradiography using a f
19 ntagonists between the beta-lactamase assay, competition-binding assay, and other direct measurements
34 d their binding affinities were evaluated in competition binding assays in HEK 293 cells transfected
38 n significantly activate the AHR, and ligand competition binding assays indicate that I3S is a direct
41 onists in [3H]5'-N-ethylcarboxamidoadenosine competition binding assays performed with yeast cell mem
48 combined with cross-linking experiments and competition-binding assays showed that the fully disorde
52 analysis and/or by [125I]alpha-bungarotoxin competition binding assays the interactions of acetylcho
54 ing affinity but similar to those shown in a competition binding assay to displace radioiodinated ana
56 We demonstrate the use of a DNA minicircle competition binding assay, together with DNA cyclization
57 nitor C protein-oligonucleotide binding in a competition binding assay under equilibrium conditions.
59 ng was assessed in mobility shift assays and competition binding assays using cisplatin-damaged DNA.
62 s and pharmacokinetic studies in mice and in competition binding assays using recombinant, soluble Fc
64 68, and (nat)Ga-JMV5132 were determined in a competition-binding assay using GRPR-overexpressing PC-3
70 etic resonance spectroscopy and protein-drug competition binding assays were employed to define the g
76 tudy ligand-protein interactions by coupling competition binding assays with mass spectrometry-based
77 ant (C1)4 and (C2)4 homotetramers along with competition binding assays with poly(A) and poly(C) indi
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