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I next assessed expression of cyclinG1, p53 target gene, after mRNA injections by visually scoring expression strength as "high" or "low" based on staining of uninjected embryos (Fig. 6B), where embryos with "high" cyclinG1 expression were inferred to be shh−/− mutant and those with "low" expression were wild-type (control stainings of wild-type embryos, not shown).
The SNP effects on gene expression were inferred by the sequences within 1 Kb upstream and downstream from the start codons because there was no information about the promoter and terminator regions in the annotations on ITAG.
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In all four cases, expression was inferred from the microarray data but could not be confirmed by real-time PCR.
In this experiment, the effect of dnPKA-GFP on p53 target gene expression is inferred from the change in proportion of embryos with stronger cyclinG1 expression.
5-HTT expression was inferred from genotype rather than measured directly and, as in all genetic-associations studies, causality cannot be asserted.
ESTs were assembled into unigene clusters that were mapped back to the O. lucimarinus Build 2.0 assembly using BLAST and the level of gene expression was inferred from the number of ESTs in each cluster.
Differential gene expression was inferred using SAM (Tusher et al. 2001) and EDGE (Leek et al. 2006).
The gene- and exon-level digital expression is inferred by the approach presented in the Methods section.
Because there are three biological replicates, presence of expression was inferred when at least two of three showed presence of expression.
Differential gene expression was inferred based on these counts using the edgeR package with common dispersion estimates [ 56], comparing each treatment (MDP and pIC) to the controls.
Gene expression was inferred by the unique mapping of 252,388 (71.49%) of the raw reads to the fullest assembly (including all assembled contigs as a "filter"; total contigs/all TUGs in Table 2).
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