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NPH_5888 and NPH_5889, encoding the NcrC and NcrD subunits of naphthoyl-CoA reductase, were both upregulated during growth on naphthalene versus growth on either pyruvate or benzoate (Figure 3), confirming microarray results showing specific induction of genes encoding benzoyl-CoA reductase during growth on naphthalene.
Similar to the microarray results showing differentially expressed genes in the WAT of HFD-fed mice after 8 weeks [24], many of the WAT proteins identified were also found to be down-regulated in HFD-fed mice, among which included enzymes involved in lipid metabolism (e.g. FAS and transketolase) and detoxification processes, as well as cytoskeleton structural components.
Our RT-qPCR measurements in the same 20 samples confirmed the microarray results, showing that this microRNA is indeed down-regulated (FC = −9.4, P = 1.6 7), and a close-to-perfect separation is shown with an AUC of 0.99 (Figure 7).
Probe sets potentially detecting NAT were validated in silico, and microarray results showing expression of NATs were confirmed by strand-specific RT-PCR.
qRT-PCR confirmed these microarray results, showing that mtl-2 was up-regulated by all HgCl2 treatments and down-regulated by MeHgCl.
Real time quantitative PCR supports previous microarray results showing COX5A is expressed in cerebral cortical tissue at a higher level in human than in chimpanzee or gorilla.
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Microarray results showed that upregulated genes were associated with an activated immune response.
The microarray results show that our modified technologies are useful to enhance sensitivity and specificity of arrays, identify expression patterns within different cells, and discover differential expression of sRNAs during the differentiation process of bone marrow stem cells.
The microarray results showed that many genes involved in cell survival and proliferation were regulated by bFGF.
Expression data from our microarray results show high levels of miR-23a throughout the GP to OL stages.
Our microarray results showed significant upregulation of master cardiac transcriptional regulators, as well as cardiac-specific structural and functional genes (Figure 2a, also see Supplemental Results S1).
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