Sentence examples for microarray profiling reveals from inspiring English sources

Global microarray profiling reveals deficiencies in ECM gene expression in PKCα−/− skin correlating with abnormal collagen fibril morphology, disorganized dermal architecture, and reduced skin strength.

DNA microarray profiling revealed a lower expression of neuron-derived orphan receptor-1 (NOR-1) in elongated SMCs.

On the other hand, microarray profiling revealed activation of multiple mucosal defence processes.

As in the case of RNA-seq, microarray profiling revealed high inter-individual Pearson correlation of the mRNA transcripts.

Indeed, microarray profiling revealed extensive changes in AtPum transcript expression patterns in response to various external stimuli (Table 1).

Our microarray profiling revealed that the expression of RBBP4, BMYB, and FOXM1 was significantly downregulated following MEIS2 depletion (Supplementary Tables S2 and S4).

Bioinformatic analysis of the microarray profiling revealed significant similarity in the genes altered in expression following treatment with the two HDACi tested within each cell line.

A microarray profiling revealed 21 upregulated miRNAs clustered on chromosome 12, including miR-433 and miR-127, in Shp − / − mice 10, 12, 13, 20, 21, 22.

Time-course microarray profiling revealed early and prolonged up-regulation of inflammation and immune system associated genes in the epididymal WAT depot and the smaller mesenteric WAT depot.

Similarly, microarray profiling revealed normal expression of EGF family receptors (EGFRs) (Supplementary Table S1), but Map3k1 mPHD ES cells have significantly impaired JNK and p38 activation after EGF stimulation (Fig 2B).

Autoantigen microarray profiling revealed that pristane-treated IFNAR2-/ mice lacked autoantibodies directed against components of the RNA-associated autoantigen complexes Smith antigen/ribonucleoprotein (Sm/RNP) and ribosomal phosphoprotein P0 (RiboP).