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Using the site-directed mutagenesis analysis, we confirmed that Q189 at the peroxidase site of COX II is essential for bioflavonoids to bind and re-activate its catalytic activity.
To simplify the mutagenesis analysis, we made use of the p48 pancreatic AID expression model to take advantage of the known low complexity transcriptome of acinar cells (MacDonald et al, 2010).
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In summary, according to the mutagenesis analysis and sequence comparisons, we suggest that electrostatic effects are responsible for the differential binding affinities between AZ and ODC and between AZ and AZI.
To validate the crystallographic observations and evaluate the significance of individual interaction, we performed mutagenesis analysis on both sides of the PP2A B56 and BubR1 interface.
To address this apparent inconsistency and further elucidate the relationship between structure and HBGA binding patterns, we performed mutagenesis analysis on the role of the three conserved sites in HBGA binding of the Boxer virus.
To further elucidate the differences and similarities between the two HBGA-binding interfaces and modes, we extended such mutagenesis analysis to the Norwalk virus.
These results are consistent with the base pairing patterns we mapped through mutagenesis analysis (Shao and Bassler, 2012).
We show by mutagenesis analysis and RNA interference that the G tracts are splicing silencers and a group of the associated exons are controlled by the G tract binding proteins hnRNP H/F.
Using X-ray crystallography, shotgun reversion/replacement scanning mutagenesis, and computational analysis, we describe, in molecular detail, a process by which extrainterfacial regions of a protein complex can be rationally manipulated to significantly improve protein engineering outcomes.
Using mutagenesis and structure analysis, we also reveal residues that are critical for the biological activity of HicA and suggest a function for the toxin in RNA degradation.
We also performed in silico mutagenesis analysis to characterize the effects of oncogenic mutations on the negative regulators and to observe the cellular outcome (whether there is/is not inflammation).
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