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After successful incorporation of HIV genes we next sought to verify expression of our transgene and capsid incorporation at the protein level by Western blot analysis.
Using this list of genes, we next determined the genes that were able to discriminate normal hematopoietic and non-hematopoietic cells by using significance analysis of microarrays (SAM).
Since neuronal differentiation is initiated by proneural genes, we next examined whether knockdown of Her8a also affect the expression of proneural markers, neurogenin1 and zash1.
After finding a correlation between menin and RNAPII association with DNA damage response genes, we next wanted to look at the effects DNA damage would have on menin localization.
Given the tumor-specific demethylation pattern seen for our target genes, we next wanted to determine if demethylation of the promoter regions of these genes occurred in a coordinated fashion within tumor samples.
To formally test the coordinate expression of these genes, we next constructed a p-value matrix derived from the Pearson's correlation coefficients calculated between the expression levels of each target (Figure 4B).
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Since distal polyA (pA) site of one gene in tail-to-tail S-AS gene pair always stayed on the way of the transcription of the other gene, we next examined the correlation between change of NATs expression and the distal pA site usage of the sense gene by PA-seq, which can quantify both the distal/proximal pA site usage and the relative gene expression level (Ni et al., 2013).
Because BUB3.2 was not a cell cycle regulated gene, we next focused on BUB3.1 candidate gene.
Having demonstrated the occupancy of ΔNp63 to Hs II of the K5 gene, we next investigated whether this segment could function as an enhancer element.
Since the divergence of the sequences of lamprey Hha and Hhb genes suggest an ancient duplication of a Shh/Ihh-like gene, we next asked whether their expression would differ too.
To assess whether KLF13 directly activates the PPARγ and C/EBPα gene, we next predicted the binding of KLF13 to the promoters of PPARγ and C/EBPα gene.
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