Therefore, we decided to first focus on the transitional patterns that can be identified from a "normally aging" to an "AD-severe" gene expression profile in hippocampus.
Here we show that under severe hypoxia, gene expression of ubiquitously expressed key enzymes and transporters in folate metabolism and nucleoside homeostasis is downregulated.
In the placenta, perturbation of methylation was less severe, and gene expression changes were more moderate.
Despite the rather severe phenotype, gene expression changes in these mice were quite modest, but, as is shown by GSEA (Fig. 7D), correlated extremely well with gene expression changes in the irradiated embryonic brain.
The sample degradation was consistently more severe in gene expression profiles when total RNA was processed for microarray analysis directly after isolation with TRIzol only (method B) [see Additional File 1, Supplementary Figure 1].
Deletion of Ada1, an adaptor protein necessary for the structural integrity of SAGA, led to a more severe diminution of gene expression of ADH2 and FBP1, as well as reductions in expression of ADY2 and JEN1 suggesting that SAGA is important for appropriate gene expression both in its capacity as a HAT as well as another, non-HAT function.
Under severe stress conditions gene expression decreases [ 4].
Here we investigated the effects of severe hypoxia on gene expression, exon splicing, and phenotype of human (h) MSCs.
Indeed, mutations that affect RSC activity display severe defects on gene expression of stress genes and mostly abolish nucleosome remodelling at the stress loci.
Using the same cell line we had previously demonstrated a modest gain of DNA methylation (at 100 days in culture) with severe consequences on gene expression [ 8].
