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Candidate gene approaches to identify contributory genes are based on prior knowledge of gene protein function.
The sequences of the synthetic genes are based on naturally occurring polyketide synthase genes but they are redesigned by custom‐made software to optimize codon usage to maximize expression in E. coli and to provide a standard set of restriction sites to allow combinatorial assembly into unnatural enzymes.
Note that ranking scores for genes are based on their differential expression between untreated and drug treated samples.
The more robust genetic predictions used to identify these additional DOX resistance genes are based primarily on synthetic lethality or fitness interaction data [101], [102], [55].
Currently, most genetical genomics studies searching for cis-regulatory genes are based on association tests between individual SNPs and expression phenotypes.
Because all other approaches suggested so far to predict periodic genes are based on statistical tests comparing differences in signal shapes of time series data from microarray experiments [13], [14], [15], [24], [16], [17], [18] we first define some terms for clarification.
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The selection of these genes was based on gene ontology and WWW.expasy.org was applied (Swiss proteomics).
Their selection of genes is based on published papers, their nutritional guidance usually the latest from the American Heart Association.
Selection of the endogenous control genes was based on previous research investigating gene expression in neutrophils.
The selection of candidate reference genes was based on either previously published transcriptomic data for R. opacus3 or literature for other Rhodococcus spp.19,20.
The physical positions of BB resistance genes were based on the published position of cloned genes.
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