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Gene expression analysis of mouse intestinal cells that lack Cdk8

ABSTRACT: RNAseq is performed (50bp single end reads) on parental young adult mouse intestinal cells (YAMC) or two clones in which Cdk8 allele is ablated using CRISPR

ORGANISM(S): Mus musculus

PROVIDER: GSE71385 | GEO | 2015/07/31

SECONDARY ACCESSION(S): PRJNA291076

REPOSITORIES: GEO

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Gene expression analysis of mouse intestinal cells that lack Cdk8

Project description:RNAseq is performed (50bp single end reads) on parental young adult mouse intestinal cells (YAMC) or two clones in which Cdk8 allele is ablated using CRISPR Examination of transcriptomic changes after knockout of Cdk8 using CRISPR. Two clones of Cdk8 knockouts are compared to parental YAMC cells

2015-07-31 | E-GEOD-71385 | biostudies-arrayexpress

Transcription profiling by array of Dictyostelium discoideum cdk8- cells and parental cells

Project description:In order to identify genes regulated by Cdk8, we performed microarray analysis to compare the expression profile in cdk8- cells with parental cells. This analysis suggested that the cdk8- strain previously described contained genome duplications; this was confirmed by directly comparing labelled genomic DNA of affected and control cell lines. Regeneration of the strain in a background lacking the gene duplication generated strains with identical defects in growth and early development, but a milder defect in spore generation, suggesting that the severity of this defect depends on the genetic background. Proteomic analysis revealed two potential targets for Cdk8 regulation, one at the transcriptional and one at the post-transcriptional level.

2010-12-03 | E-TABM-1013 | biostudies-arrayexpress

Next Generation Sequencing Quantitative Analysis of Wild Type, CDK8-/-, CDK19-/-, and CDK8-/-CDK19-/- mouse instestinal organoids transcriptomes

Project description:Purpose: The goals of this study were to compare gene expression profiles of mouse intestinal epithelium organoids with intact or disrupted CDK8 and CDK19 genes. Methods: mRNA profiles of all organoid genotypes, in biological triplicates, were generated by deep sequencing using the BGISEQ SE50 50 million single-end, 50bp reads per sample. The sequence reads that passed quality filters were aligned to the mouse genome, quantified, and differential gene expression (DGE) analysis was performed using DEseq2. Results: Using an optimized data analysis workflow, we mapped about 50 million sequence reads per sample to the mouse genome (GRCm38.p6) and identified differentially expressed genes. This mild changes in overall gene expression, preferentially enriched in tissue specif genes. The transcription profile showed an overlap between those present in a CFTR KO context. Conclusions: CDK8/19 knockout causes tissue specif expression alteration. Intestinal organoids presented a CFTR-like phenotype after removal of both genes

2022-10-23 | GSE186377 | GEO

Assessing the impact of Ccnc or Cdk8 loss +/- ATR inhibition on mRNA gene transcription using RNA-seq

Project description:We have found that loss of Ccnc or Cdk8 (members of the RNAPII mediator complex) provide ATRi resistance. As part of invesitgations into the mechanism of this suppression, we probed for specific changes in the transcriptome by performing RNA-seq in WT, Cdk8 KO and Ccnc KO mESCs following DMSO or ATRi (AZD6738) treatment. However, this did not identify any transcripts that were significantly differentially regulated following AZD6738 treatment in both Ccnc and Cdk8 KO, but not WT, cells. Similarly, pathway analyses of proteins whose transcripts were up- or down-regulated in a treatment-independent manner in both Cdk8 and Ccnc KO clones compared to WT mESCs did not provide a clear explanation why the Ccnc/Cdk8 KO cells are ATRi resistant.

2021-07-12 | GSE165359 | GEO

CDK8 knockdown in HT-29 cells and CDK8 & MED12 knockdown in R1 cells

Project description:This SuperSeries is composed of the following subset Series: GSE30815: CDK8 knockdown in HT-29 human colon cancer cells GSE30816: CDK8 and MED12 knockdown in R1 mouse ES cells Refer to individual Series

2012-03-05 | E-GEOD-30817 | biostudies-arrayexpress

Gene expression for transformed YAMC clones

Project description:YAMC murine colonic epithelial cells were repeatitively treated with commensal bacteria-polarized macrophages or 4-HNE. Following 10 treatments, 25 clones were selected to engraft immunodeficient mice, and 10 out of 25 clones grew tumors in these mice. To explore gene expression associated with cellular transformation, whole-genome profiling was performed on 10 transformed clones and compared with untreated YAMC controls using Illumina Mouse WG-6 v2.0 Expression BeadChip.

2014-07-03 | GSE55233 | GEO

Gene expression for transformed YAMC clones

2014-07-03 | E-GEOD-55233 | biostudies-arrayexpress

Effects of CDK8/19 Mediator Kinase inhibition on gene expression in castration-resistant prostate cancer cell line 22Rv1 and its derivatives grown in vitro.

Project description:RNA-Seq analysis was carried out to investigate the effects of selective CDK8/19 inhibitor SNX631 on gene expression in different 22RV1 derivatives grown in cell culture, under androgen-supplemented and androgen-deprived conditions. The 22Rv1 derivatives were generated as following: Parental 22Rv1 (Rv1-WT) were transduced with a lentivirus expressing luciferase, yielding the derivative Rv1-Luc. 22Rv1 cells with a double knockout of CDK8 and CDK19 (Rv1-dKO) were made via CRISPR/Cas9. Rv1-dKO cells were further transduced with lentiviruses to generate Rv1-dKO re-expression derivatives that express wild-type CDK8 or CDK19 (Rv1-dKO-CDK8 or Rv1-dKO-CDK19) and kinase-inactive D173A mutants (Rv1-dKO-CDK8M or Rv1-dKO-CDK19M).

2024-03-31 | GSE240369 | GEO

Transcriptomic analysis of the in vivo effects of CDK8/19 inactivation in 22Rv1 xenografts growing in intact and castrated NSG mice

Project description:RNA-Seq analysis was carried out to investigate the effects of CDK8/19 inactivation in the tumors formed in intact and castrated NSG mice by different 22Rv1 derivatives, with or without SNX631 treatment. The 22Rv1 derivatives were generated as following: Parental 22Rv1 (Rv1-WT) were transduced with a lentivirus expressing luciferase, yielding the derivative Rv1-Luc. 22Rv1 cells with a double knockout of CDK8 and CDK19 (Rv1-dKO) were made via CRISPR/Cas9. Rv1-dKO cells were further transduced with lentiviruses to generate Rv1-dKO re-expression derivatives that express wild-type CDK19 (Rv1-dKO-CDK19) and the kinase-inactive D173A mutant (Rv1-dKO-CDK19M). SNX631 is a selective and orally bioavalable CDK8/19 inhibtor.

2024-03-31 | GSE240370 | GEO

IL6-regulated CDk8-mediated phosphoproteome of human primary Th1 cells

Project description:Cytokines are highly pleiotropic ligands that critically contribute to a balanced immune response. We have an incomplete understanding of how cytokines elicit their functional pleiotropy, which has limited their therapeutic efficacy. Here, using Interleukin-6 (IL-6) as a model system, we have performed detailed phosphoproteomic and transcriptomic studies in human CD4 + T helper (Th)-1 cells to address the molecular bases defining cytokine functional pleiotropy. We have identified cyclin dependent kinase (CDK)8 as a new negative regulator of transcriptional activities of signal transducer and activator of transcription (STAT)3. We found that CDK8 is a major regulator of the IL-6 phosphoproteome and interacts with STAT3 in the nucleus upon IL-6 stimulation. Inhibition of CDK8 activity, using specific small molecules inhibitors, reduced the IL-6-induced phosphoproteome by 23% in Th-1 cells, including STAT3 S727 phosphorylation. STAT3 binding to target DNA sites in the genome was increased upon CDK8 inhibition, which resulted in a concomitant increase in STAT3 mediated transcriptional activity. Importantly, inhibition of CDK8 activity under Th-17 polarizing conditions resulted in an enhancement of Th-17 differentiation. Our results support a model where CDK8 regulates STAT3 transcriptional processivity via modulation of its gene loci resident time, critically contributing to diversification of IL-6 responses.

2020-12-23 | PXD020964 | Pride

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