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p53 DNA binding was studied in seven-day differentiated PC12 cells via chromatin immunoprecipitation (ChIP) analysis.
The effect of interactions between urban air particulates (UAP) and carcinogens on bioavailability, metabolism, and DNA binding was studied in the isolated perfused and ventilated rat lung.
Binding was studied in the presence of the inhibitor L-Phe-Gly-Gly or the control peptide L-Gly-Gly-Gly along with the substrate pNPP.
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The functional consequences of uncoupling PC1/Gα12 binding were studied in apoptosis assays utilizing HEK293 cells with inducible PC1 overexpression.
The role of DNA methylation in cDDP binding was studied using methylated and unmethylated plasmid incubated in vitro with cDDP.
A "knock in" mouse harbouring a TRβ mutant defective in DNA binding was studied [18].
The binding behavior was studied in CH3CN using 1H NMR, fluorescence and UV vis spectroscopic methods.
Using these lines, the nature of integrin binding sites was studied in order to delineate the bioactivity of different collagen substrates.
In terms of receiver design, an optimal receiver design based on weighted sum detectors was proposed in [19], and a ligand-binding reception model was studied in [20].
Therefore, the expression of inhibin/activin subunits, of activin receptors and of the activin-binding protein follistatin was studied in testicular germ cell tumours, using RNAase protection assays.
The albumin-derived peptide which most potently reduced the binding of In-minigastrin and In-exendin in the cell binding assay, peptide #6, was studied in rats according to the same procedure.
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