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To determine the exact location of VL12.3 binding we used a 3 AA stepped peptide array binding assay (Fig. 6A).
To verify the specificity of GATA2-Zf binding, we used a canonical GATA-RE in the new fluorescence anisotropy assays (Fig. 6) (Table 2).
To test whether HOT1-dependent telomere elongation indeed requires DNA binding, we used a HOT1ΔHomeobox variant.
To evaluate whether other domains of Pan3 contribute to RNA binding, we used a short synthetic RNA that could be more readily quantitated.
To determine the threshold of miRNA target prediction based on complementary binding, we used a simulated control database with the size of Giardia genome.
To identify the domain of JDP2 that is involved in ARE binding, we used a series of deletion mutants of JDP2 and examined their binding to the ARE.
Similar(51)
To investigate the consequences of acetylation on ADP binding, we used an ensemble docking approach.
Thus, to analyse p53 binding we used an amplicon −700 bp, which is located between the promoter fragments 1 and 2. It should be noted that miR-16-2 is coded by an intronic gene, located within the SMC4 (structural maintenance of chromosomes) gene.
To investigate the characteristics of binding we used SPR, a method that can detect the interaction of mAb immobilized on a sensor chip with a small antigen such as a peptide, thus avoiding avidity contributions and allow examination of the kinetics and thermodynamics of Ab-Ag complex formation.
To measure CREB binding, we used HaloCHIP, an antibody-free alternative to the ChIP method that utilizes the HaloTag fusion protein, and also high-throughput promoter-luciferase reporter assays, which provide rapid and quantitative screening of promoters for transcriptional activation or repression in living cells.
For Vg1RBP/Vera binding, we used the pVLE plasmid, a gift from Dr Nancy Standart, linearized with MscI (51).
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