We set out to correlate microRNA transcription to cell-specific growth-rate by microarray analysis of 5 CHO suspension cell lines with low to high specific growth rates.
In this study, we investigated whether C3 deficiency can be diagnosed in neonates by microarray analysis of DBSS.
RISC mRNA and miRNA components were profiled by microarray analysis of malignant human U-87 astrocytoma cells and its non-malignant counterpart, primary human astrocytes.
These type I IFN IRGs were identified by microarray analysis of fibrosarcoma, epithelial, or endothelial cell lines treated with IFN-α or IFNβ [22], [23].
In order to evaluate its role in F. novicida, we monitored expression of nine genes identified by microarray analysis of a F. tularensis LVS hfq mutant [13].
We examined HBD2 mRNA expression at three colonic locations by microarray analysis of biopsies from 151 patients (53 CD, 67 ulcerative colitis [UC], 31 controls).
The confirmation of the differential expression pattern obtained by microarray analysis of five miRNAs by Taqman qRT-PCR excluded the possibility that the high variability among samples was technical.
Changes in expression, as assessed by microarray analysis, of BCL2, EPHA4 and EPHA3 were validated by real time PCR in each MSC population and confirmed the microarray observations (Figure 2).
Very low levels of always early and cookie monster are suggested by microarray analysis of various tissues [24], but RT-PCR or northern blots of gonadectomized or germline-less adult males failed to detect them [18], [25].
The molecular basis for the phenotypic differences was also investigated by microarray analysis of sessile versus planktonic opaque and transparent variants, and the role of candidate biofilm-associated genes in pathogenesis was evaluated in a mouse infection model.
Efforts have been made to identify the genes involved in pathogenesis at various stages of the disease in both in vivo and in vitro models by microarray analysis of brain tissue [2] [6].
