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. Author manuscript; available in PMC: 2013 Oct 1.
Published in final edited form as: Pharmacogenomics J. 2011 Dec 13;13(2):121–129. doi: 10.1038/tpj.2011.55

Figure 2.

Figure 2

a) Volcano plots show the mean log2 fold change (dex/vehicle) and corresponding evidence of differential expression (−log10 p-value) for each gene (represented by a single point). Plots for response after 8h and 24h are shown separately. Transcriptional response is widespread, includes both up- and down-regulated genes and increases in intensity with duration of treatment. b) Boxplots show examples of genes with large responses to dex treatment, the well characterized GR target glucocorticoid-induced leucine zipper (GILZ, log2 fold change = 2.8, p = 1.4×10−15) and the anti-apoptotic TNF-receptor TNFRSF4 (log2 fold change = −1.6, p = 2.6×10−12). Dots in a) corresponding to these genes are colored in blue. c) Boxplots show examles of genes with small, but consistent responses to dex treatment, the mitogen induced gene ERRFI1 (log2 fold change = −0.10, p = 4.4×10−3) and the apoptosis-associated RAD51 family member RAD51B (log2 fold change=0.096, p=8.4×10−3). Dots in a) corresponding to these genes are colored in red. d) A Venn diagram shows the overlap between differentially expressed genes in PBMCs, LCLs and osteoblasts at an FDR<0.01. Counts only reflect genes expressed in all three tissues.