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For each mutant, we determined the minimum inhibitory concentration (MIC) of CTX and CAZ in triplicate.
To test whether the ces-D-specific phenotypes correlate with altered BR levels in the mutant, we determined BR amounts by GC/MS.
To explore the molecular basis of the effects of this double mutant, we determined the J-1N-EGF3 structure from crystals grown at a physiological pH in the presence of 7.5 mM Ca2+ (Table 1).
In COX-2MECKO mice transgenic for an activated ErbB2 mutant, we determined delayed tumor onset and reduced tumor multiplicity, as well as reduced tumor vascularization, compared to wild type (WT).
To analyze the influence of chromosome size on occurrence of nonexchange chromosomes in the wild-type, msh4 –R676W, and msh4 Δ mutant, we determined the percentage of nonexchange events for each chromosome.
In conclusion, by assessing the global transcriptional response of a pst mutant, we determined that the effects of this mutation resulted in up-regulation of members of the Pho regulon, which are involved in phosphate uptake and metabolism.
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Through molecular modeling and comparative analysis of machines assembled with protein-tagged components or from different deletion mutants, we determined the molecular architecture of the secretion machine in situ and localized its structural components.
Using a collection of bacterial effector mutants, we determined that PB disassembly is dependent on the activity of the SPI-2 encoded T3SS, and identified the secreted effector protein, SpvB, as a mediator of this process.
Given the known involvement of Slbp in histone mRNA biogenesis, as well as our observations that chromatin structure and genome stability are compromised in Slbp mutants, we determined whether the total amount of histone protein in Slbp mutants is different than wt.
Along with the collection of transposon mutants, we determined the transposon insertion sites of individual mutants.
Following detailed analysis using various PKC δ mutants, we determined that PKC δ activation was mediated by caspase-dependent proteolysis.
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