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Exact(9)
Association between the different mutations was tested using Fisher's exact test.
The different percentile of each set of mutations was tested against that of documented disease-causing mutations.
Whole exome sequencing (WES) was performed in the index case from each family and co-segregation of candidate pathogenic mutations was tested by Sanger sequencing.
The tributyrin hydrolysis activity of wild type LesB and LesBMUT1/LesBMUT2 with suggested mutations was tested in vitro using heterologous expression of these proteins in E. coli.
A subset of these identified mutations was tested by PCR amplification from the original (non-pooled) DNA samples using locus-specific primers.
The impact of the stability of LKB1 mRNA on detecting LKB1 mutations was tested using RT PCR with mRNA extracted from NSCLC cell lines that had previously been characterised for LKB1 mutations.
Similar(51)
The effects of these mutations were tested using neuropeptide Y receptors Y1R and Y2R.
Effects of those mutations were tested with the CPM assay and the affinity MS assay (Table 2).
The deleted mutations were tested in mice for attenuation in virulence and for growth in macrophages.
In the infection complementation assay, the A73D and A74D mutations were tested individually and in combination.
Piwi2/2, piwi3/3, and transheterozygous piwi3/2 mutations were tested in these experiments.
More suggestions(15)
transfer was tested
mutations was detected
mutations was confirmed
mutations was coupled
mutations was determined
mutations was followed
mutations was carried
mutations were tested
mutations was observed
mutations was introduced
mutations was calculated
mutations was identified
mutations was verified
mutations was analyzed
mutations was based
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