23 research outputs found

    Integrated Left Ventricular Global Transcriptome and Proteome Profiling in Human End-Stage Dilated Cardiomyopathy - Fig 7

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    <p>Venn diagrams representing overlap of (A) predicted upstream regulators, (B) enriched GO biological processes, and (C) KEGG pathways between differentially expressed genes and proteins.</p

    Functional interaction network of 16 genes.

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    <p>Genes were clustered according to their associated pathways, which are shaded with a different color. Green nodes indicate down-regulated, red, up-regulated, and linker genes (non-colored nodes). The edges represent interactions between genes, with arrows indicating directed interactions and dotted lines indicating predicted relationships.</p

    Gene interaction network analyses of 16 commonly dysregulated proteins/genes based on the Ingenuity knowledge base.

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    <p>Green indicates down-regulated, and red, up-regulated. The color intensity is correlated with fold change. Straight and dashed lines represent direct or indirect gene to gene interactions, respectively.</p

    Validation analyses using independently performed microarray and RNAseq datasets.

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    <p>(A) <b>The PCA and (B) unsupervised hierarchical clustering using our 16 gene set discriminated individuals as DCM and controls in Barth et al.’s [<a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0162669#pone.0162669.ref016" target="_blank">16</a>] microarray data</b>. Samples are in the columns and genes are in the rows (gene symbols are listed on the right). The expression level of each gene across samples is scaled to [−3, 3] interval. The expression levels are depicted using a color scale as shown at the top of the figure. (C) <b>PCA analysis using RNA-Seq dataset for (non-ischemic cardiomyopathy (NICM) (n = 8) and normal controls (n = 8) from Yang et al [<a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0162669#pone.0162669.ref026" target="_blank">26</a>].</b> (D) <b>Venn diagram representing the genes common to DEGs in our DCM patients (Colak et al[<a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0162669#pone.0162669.ref015" target="_blank">15</a>]) with DEGs in validation datasets from datasets from Yang et al [<a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0162669#pone.0162669.ref026" target="_blank">26</a>] and Liu et al [<a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0162669#pone.0162669.ref023" target="_blank">23</a>] for RNA-Seq data for independent samples from human failing heart</b>.</p

    p16 modulates apoptosis through E2F1.

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    <p>(A) Western blots showing the expression of the indicated pro-and anti-apoptotic proteins in U2OS and EHI. (B) Western blots showing the expression of the indicated proteins in U2OS, U2OS cells stably transfected with plasmids encoding either scrambled sequence (ctl) or E2F1 (+). The numbers below the bands indicate the corresponding expression levels. (C) U2OS, EH1 and E2F1-expressing U2OS cells were either mock-treated or challenged with doxorubicin (2 µM) and then re-incubated for 72 hrs. Cells were then divided into two groups; one was used to analyze cell death by annexinV/PI flow cytometry. The numbers in the charts indicate the proportions of early and late apoptosis. (D) Histogram showing the proportions of apoptosis (early+late) induced by different doses of doxorubicin. The error bars represent standard deviation of three different experiments. (E) The second group of cells was used to assess the level of the indicated proteins by immunoblotting. (F) Graph showing the Bax/Bcl-2 ratio in the indicated cells after treatment with doxorubicin. Error bars represent standard deviation of at least three different experiments.</p
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