Browse
Submit Data
Databases
API
Help

Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

43 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

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 Examination of transcriptomic changes after knockout of Cdk8 using CRISPR. Two clones of Cdk8 knockouts are compared to parental YAMC cells

ORGANISM(S): Mus musculus

SUBMITTER: Florian Gnad

PROVIDER: E-GEOD-71385 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

ACCESS DATA

Json Xml

Similar Datasets

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

2015-07-31 | GSE71385 | GEO

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

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

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

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

Inhibition of CDK8 Mediator Kinase Suppresses Estrogen Receptor Signaling and Growth of Estrogen Receptor Positive Breast Cancer

Project description:Hormone therapy targeting estrogen receptor (ER) is the principal treatment for ER-positive breast cancers but many cancers develop resistance to anti-estrogens. Cyclin-dependent kinase 8 (CDK8) is a transcriptional regulator of several oncogenic pathways. Expression levels of CDK8 and ERα are inversely correlated in breast cancers suggesting a functional association between CDK8 and ER. CDK8 inhibition by selective small-molecule inhibitors, by shRNA knockdown or by CRISPR-Cas9 knockout suppressed estrogen-induced transcription, with no significant effects on ERα protein expression or phosphorylation. CDK8 inhibition also abrogated the mitogenic effect of estrogen on ER-positive breast cancer cells and potentiated growth inhibition by the ER antagonist fulvestrant. In vivo, administration of a CDK8 inhibitor suppressed ER-positive breast cancer xenograft growth and augmented the effects of fulvestrant with no apparent toxicity. CDK8 inhibitors also suppressed the development of estrogen independence in ER-positive breast cancer cells. These results identify CDK8 as a novel drug target for breast cancer therapy.

2017-02-14 | GSE93193 | GEO

Transcriptomic analysis of transformed murine hepatic progenitors depleted or not for CDK8 or CDK19 kinases

Project description:We report transcriptomes of hepatic progenitors cells (BMEL) wild-type or transformed by the expression of H-RasG12V, depleted of CDK8 or CDK19 kinases by crispr/Cas9 mediated editing.

2019-10-14 | GSE138808 | GEO

RNA sequencing of Control, Î?Cop1Î², Î?Cop1Î² and Î?Cop1Î² Î?ETV1/4/5Î² islets

Project description:Identify genes which are differentially expressed in Î?Cop1Î² compared to control islets and are also signficantly rescued in Î?Cop1Î? Î?ETV1/4/5Î² Islets were harvested from 5 biological replicates of the followig genotypes: Control, Î?Cop1Î² and Î?Cop1Î? Î?ETV1/4/5Î². Islets were individually handpicked and total RNA was isolated and purified for library preperation and Next Generation Sequencing.

2015-11-09 | E-GEOD-70788 | biostudies-arrayexpress

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data