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Effects of Inhibition of CDK8/19 Mediator Kinase by Senexin B in HCT116 cells treated with or without TNF-alpha

ABSTRACT: We have investigated the effects of CDK8/19 inhibitor Senexin B on NFκB-mediated transcription, induced by a canonical NFκB activator, TNFα.

ORGANISM(S): Homo sapiens

PROVIDER: GSE101628 | GEO | 2017/08/18

SECONDARY ACCESSION(S): PRJNA395029

REPOSITORIES: GEO

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Effects of Inhibition of CDK8/19 Mediator Kinase by Senexin A in HEK293 cells treated with TNF-alpha II

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Effects of Inhibition of CDK8/19 Mediator Kinase by Senexin A in HEK293 cells treated with TNF-alpha I

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Effects of Inhibition of CDK8/19 Mediator Kinase by Senexin B in HEK293 cells treated with or without TNF-alpha

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Effects of CDK8/19 Mediator Kinase inhibition by Senexin B on gene expression in HEK293 cells

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Effects of CDK8/19 Mediator Kinase inhibition by Senexin B in HEK293 cells treated with or without Interferon-gamma

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Transcriptomic analysis of the effects of CDK8 and CDK19 knockout and re-expression and selective CDK8/19 kinase inhibitor Senexin B treatment on gene expression in HEK293 cells

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Effect of CDK8/19 inhibitor Senexin A on p21-regulated gene expression in human HT1080 p21-9 cells with IPTG-inducible p21

Project description:p21 (CDKN1A) expression from an IPTG-inducible promoter in HT1080 p21-9 cells was previously shown to inhibit a set of genes, many of which are involved in cell cycle progression, and to upregulate another set of genes, some of which have been implicated in cancer and age-related diseases. We have now developed Senexin A, a small-molecule inhibitor of p21-induced transcription, which we found to be a selective inhibitor of CDK8 and CDK19. Here we tested the effect of Senexin A on the induction and inhibition of transcription by p21. In this dataset, we include microarray gene expression data from samples of HT1080 p21-9 cells that were either untreated, treated with p21-inducing IPTG alone, with Senexin A alone, or with IPTG and Senexin A. This experiment shows that Senexin A inhibits primarily the induction but not the inhibition of gene expression by p21. The data for each of the four samples were normalized to the sample from untreated cells, using GeneSpring GX. Fold changes in gene expression upon the addition of IPTG with or without Senexin A were compared using Microsft Excel. Changes in the expression of specific GO categories of genes were compared using GeneSpring.

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