Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

PolyA RNA-seq from HCT116 (WT and CDK8as/as) cells in normoxia or hypoxia and treated with DMSO or 3MB-PP1

ABSTRACT: To determine the impact of CDK8 kinase activity on steady-state mRNA levels, we performed RNA-seq analysis of colorectal carcinoma cell line HCT116 (CDK8wt/wt and CDK8as/as) in the presence of absence of 3MB-PP1 to specifically inhibit analog senstitive (as) CDK8.

ORGANISM(S): Homo sapiens

PROVIDER: GSE101526 | GEO | 2017/11/07

SECONDARY ACCESSION(S): PRJNA394729

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Similar Datasets

PolyA RNAseq from HCT116 cells in normoxia and hypoxia

Project description:To determine the effects of depleting TIP60, CDK8, or HIF1A on the transcriptional response to hypoxia, we performed RNAseq analysis of four HCT116 colorectal carcinoma cell lines (shNT, HIF1A-/-, shTIP60 and shCDK8) in normoxic and hypoxic (24hrs, 1% O2) conditions. PolyA RNA for two independent biological replicates was purified from HCT116 cells stably expressing an shRNA against a non-targeting control (shNT), TIP60 (shTIP60) or CDK8 (shCDK8), or genetically deleted HIF1A (HIF1A-/-) subjected to 24hrs 1% O2 (hypoxia) or maintained under ambient oxygen (21%; normoxia) was sequenced on the Ion Torrent platform. Reads were aligned to the human genome and gene-level counts were used for differential expression analysis.

2016-06-02 | E-GEOD-68297 | biostudies-arrayexpress

PolyA RNAseq from HCT116 cells in normoxia and hypoxia

2016-06-02 | GSE68297 | GEO

Proteome after 3MB-PP1 treatment

Project description:The human cytomegalovirus (HCMV) is a member of the beta-herpesvirus family and inflicts life-long latent infections in its hosts. HCMV has been shown to manipulate and dysregulate many cellular processes. On major interactor with the cellular host is the viral kinase pUL97. The UL97 gene is essential for viral replication and kinase-deficient mutants of pUL97 display a severe replication defect. Recently, another group established an analog-sensitive version of the pUL97 protein. This mutant kinase can be treated with a non-hydrolysable ATP analog, thereby inhibiting its kinase function. This process is reversible by removing the ATP analog by media change. We introduced this mutant version of the pUL97 protein into the laboratory strain Ad169 of HCMV, BADwt, creating a BAD-UL97-as1 viral mutant. This mutant virus replicated normally in infected cells in the absence of the ATP analog and maintained its ability to phosphorylate its cellular substrates. However, when treated with the ATP analog, BAD-UL97-as1 displayed a defect in the production of intra- and extracellular viral DNA and in the production of viral progeny. Furthermore, in the presence of 3MB-PP1, the well-established substrate of pUL97, the retinoblastoma protein (Rb) was no longer phosphorylated. This effect was detectable as early as 4 hours post treatment, which allows for studies on pUL97 without the complication of low viral titers. Nevertheless, we observed off-target effects of 3MB-PP1 on several cellular processes, which should be considered with this approach.

2023-03-11 | PXD036455 | Pride

CDK8 ChIP-seq from HCT116 cells in normoxia and hypoxia

Project description:To test if CDK8 acts directly at HIF1A target genes, we performed ChIP-seq experiments in HCT116 cells under normoxic and hypoxic conditions. ChIP-seq for CDK8 versus Input under normoxia and 24hrs hypoxia (1% O2).

2013-03-01 | E-GEOD-38258 | biostudies-arrayexpress

CDK8 ChIP-seq from HCT116 cells in normoxia and hypoxia

Project description:To test if CDK8 acts directly at HIF1A target genes, we performed ChIP-seq experiments in HCT116 cells under normoxic and hypoxic conditions.

2013-03-01 | GSE38258 | GEO

Transcriptional profiling of Neurospora crassa cells containing MAK2Q100G allele: Exposure to ATP-analog (1NM-PP1) vs control

Project description:To study the consequences of MAK-2 activity modulation during vegetative cell fusion, we took advantage of a previously constructed allele of MAK-2 (MAK-2Q100G) to specifically perturb kinase signaling during germling vegetative cell fusion (inhibition of MAK-2Q100G activity by addition of the ATP analog 1NM-PP1 results in a phenotype indistinguishable from mak-2 deletion strains). Whole genome microarrays of mak-2Q100G cells following 20 min 1NM-PP1 treatment were performed. Two-condition experiment, Neurospora crassa cells containing MAK2Q100G allele treated with 1NM-PP1 inhibitor vs untreated control. Cy3 and Cy5 dye swaps were performed.

2013-06-01 | E-GEOD-46912 | biostudies-arrayexpress

Transcriptional profiling of Neurospora crassa cells containing MAK2Q100G allele: Exposure to ATP-analog (1NM-PP1) vs control

2013-06-01 | GSE46912 | GEO

Expression data from HCT116 colorectal cancer cells.

Project description:To define the contribution of CDK8 versus CDK19 to gene expression control, we performed a series of microarray assays for cells where each kinase was stably knocked down. Toward this end, we subjected HCT116 cells to three different stress stimuli: 5-fluorouracil (5FU), glucose deprivation, and hypoxia. We found that CDK8, but not CDK19, functions as a widespread coactivator of HIF1A target genes in hypoxia. Total RNA from HCT116 cells harvested using an RNeasy kit (Qiagen) was used for gene expression analysis on Affymetrix HuGene 1.0 ST arrays following the manufacturer’s instructions. Differential gene expression was determined with Partek software using one-way ANOVA.

2013-03-01 | E-GEOD-38061 | biostudies-arrayexpress

Expression data from HCT116 cells following CDK8 knockdown

Project description:We used microarrays to detail the global programme of gene expression following CDK8 knockdown in HCT116 cells

2016-09-29 | GSE87428 | GEO

24hr CA treatment vs. DMSO in HCT116 cells (from 'Identification of CDK8 and CDK19 substrates in human cells using cortistatin A and quantitative phosphoproteomics')

Project description:Cortistatin A (CA) is a highly selective inhibitor of the Mediator kinases CDK8 and CDK19. Using CA, we report here the first large-scale identification of Mediator kinase substrates in human cells (HCT116). Among over 16,000 quantified phosphosites, we identified 78 high-confidence Mediator kinase targets within 64 proteins, including DNA-binding transcription factors and proteins associated with chromatin, DNA repair, and RNA polymerase II. Although RNA-Seq data correlated with Mediator kinase targets, CA effects on gene expression were limited and distinct from CDK8 or CDK19 knockdown. Quantitative proteome analyses, which tracked about 7,000 proteins across six time points (0 â?? 24h), revealed that CA selectively affected pathways implicated in inflammation, growth, and metabolic regulation; contrary to expectations, increased turnover of Mediator kinase targets was not generally observed. Collectively, these data support Mediator kinases as regulators of chromatin and RNA polymerase II activity and suggest cellular roles beyond transcription, including metabolism and DNA repair. HCT116 cells were treated with either 100nM CA or DMSO in biological triplicate for each population (6 samples total). Treatment was for 24h for compound and vehicle.

2016-02-26 | E-GEOD-78506 | biostudies-arrayexpress

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

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