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However, DNA microarray analyses did not detect any increase in the expression of the cas genes or restriction enzymes in cells lacking another MMR gene, mutS (Supplementary Table S2).
However, microarray analyses did not reveal significant changes of such marker genes in P5 mouse heart ventricles, nor did adult Smyd2 cKO hearts exhibit differences in size or weight as would have been expected if the proliferation of cardiomyocytes was affected [55].
DNA microarray analyses did not identify differential mRNA expression of any gene as a result of E2 at any time (we could not reject the global null that E2 was independent of mRNA expression of all genes represented on the chip).
Microarray analyses did not show increase of IL-1 and TNFalpha.
Although the microarray analyses did not reveal the induction of IFN-γ gene expression itself, IFN-γ appeared at a central position in the network.
Even though microarray analyses did not suggest transcriptional modulation as an early implicated mechanism, we first explored the impact of CGs on Mcl-1 mRNA expression levels by RT-PCR to further ascertain our results.
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Microarray analyses do not reveal these expression profiles because microarray expression data are often presented in a relative scale where the extremely low abundance signals will be dwarfed by the high abundance signals.
Our data, obtained from microarray analyses, do not directly address overall levels of gene expression but instead address expression breadth among tissues or alternate phenotypic classes.
While this may indeed be the case from a statistical perspective, the fact is that the vast majority of microarray analyses do employ a normalization step prior to the calculation of correlation coefficients.
Our previous results, using microarray and proximate analyses, did not reveal any significant modification of the lipolysis pathways in atrophying rainbow trout muscle [ 4, 37].
Microarray analyses have done much to illuminate these pathways.
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