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Finally, the concept of cooperative binding is analyzed in order to underline the limitations of the pure additive calculation method based on average binding energies.
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To this end, the in vivo p53/DNA binding was analyzed in SKBR3 cells with ChIP assay.
AP-ligand binding was analyzed in sections from at least three animals across two different litters per genotype.
Indeed, when HSF1 promoter binding was analyzed in the absence of heat shock, a very different profile was uncovered and included various sets of genes related to processes such as apoptosis, RNA splicing, and ubiquitination.
The ab initio results agree well with the experimental observations, and the underlying binding mechanism is analyzed in great details.
Secondary structure and substrate binding were analyzed using CD are in good agreement with the in silico predictions.
Compounds were tested at 1 mM or 2mM each and binding was analyzed by monitoring changes in the 15N HSQC spectra.
The kinetics of binding were analyzed as previously described in detail (1, 27).
Here, we determined the crystal structures of Tir-binding domain of EHEC O157 H7 intimin at 2.8 Å, together with an Asn to Tyr mutant at amino acid 916 (IntN916Y) at 2.6 Å. Complex model of EHEC Intimin-Tir is built, and four key residues involved in their binding are analyzed.
The conservation of 17 key reference residues involved in nucleotide binding was analyzed (Fig. 4).
Ligand binding was analyzed during titration using cross-peaks in H N HSQC spectra to identify protein residues involved in binding and saturation transfer difference (STD) NMR to identify binding epitopes on the ligand.
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