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We eliminated genes for which the 70mer feature on the microarray did not demonstrate homology to any known Brassica sequence.
This indicated that assessing T cell responses against these epitopes using the cellular microarray did not provide a prediction of autoimmune status or progression.
However, the Oligo DNA microarray did not completely overcome cross hybridization.
Real-time qPCR validated the short half-life of U6 and U6atac, but not U5, for which the microarray did not predict a change.
The microarray did not identify Emr1(F4/80) as being down-regulated due to an error; however, a previous study showed this gene did show reduced expression [ 16].
The authors argue that a previous microarray did not show substantial decrease in genes of interest, but this does not imply that the epigenome is stable.
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However, it is apparent that the two platforms diverge at low expression levels, where RNA-Seq often indicates differential expression and the microarray does not.
The majority of sequencing-unique ERs occur in regions where the microarray does not have sufficient probes to confidently identify enrichment (generally, at least three probes are required).
Indeed, these microarray do not rely on a limited catalog of splicing specific probes, but instead cover a very large list of exons identified or predicted so far, thus limiting biases toward previous known AS [1], [5].
As our microarray does not contain the dosage compensation complex, the latter could not be assessed.
Considering this, the Canine 2.0 microarray does not have a probe for this gene.
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