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In most cases, incomplete coverage of these genes was due to the fact that the reference cattle gene model that was used was incomplete relative to other mammals.
The difference in the gene expression breadth between gbM and unmethylated genes was due to a higher proportion of the gbM genes (82.4 vs. 72% unmethylated genes) having a maximal expression breadth.
The goal of this study was to determine whether parasite activation of host immediate early genes was due to Toxoplasma signaling through SRF.
In order to rule out the possibility that failure to PCR amplify the pfhrp2/3 genes was due to possible polymorphisms at the primer binding sites, an additional PCR reaction was undertaken for samples that were negative for either genes using the same primers with lower annealing temperatures (down to 42°C).
The incomplete coverage of the HLA genes was due to remaining unphased regions, which may include large gaps.
Although overall expression levels are similar between strains, a relatively high number of differentially expressed genes was due to deviating gene expression levels in BL6.
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kneri using COI or a few nuclear genes is due to sampling error.
To decipher whether the decrease in endocrine-related genes is due to decreased number of endocrine cells or a reduction of transcripts per cell, the number and percentage of endocrine progenitors (NGN3+) and their derivatives (CHGA+) were quantified at different time points during transition from D9 to D23_L (Supplementary Fig. 3b f).
Sequence swapping experiments as well as calculations of predicted mRNA secondary structure provided support for the hypothesis that differential cytoplasmic expression of the E. coli optimized versus wild-type cutinase genes is due to differences in 5′ mRNA secondary structures.
The modest number of genes is due to the limited variations between the two parental genomes in the heterozygote.
The reduced ability of PGC-1beta to induce gluconeogenic genes is due, at least in part, to its inability to physically associate with and coactivate hepatic nuclear receptor 4alpha (HNF4andha) and forkhead transcription factor O1 (FOXO1), two critical transcription factors that mediate the activation of gluconeogenic gene expression by PGC-1alpha.
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