Browse
Submit Data
Databases
API
Help

Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Transcription profiling by array of Drosophila melanogaster CDK8 and Cyclin C homozygous mutants, determined using Affymetrix GeneChip Drosophila Genome 2.0 Array

ABSTRACT: Gene expression profile in CDK8 and Cyclin C homozygous mutants (the third instar larvae) is determined using Affymetrix GeneChip Drosophila Genome 2.0 Array

ORGANISM(S): Drosophila melanogaster

SUBMITTER: Jun-yuan Ji

PROVIDER: E-MTAB-1066 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

ACCESS DATA

Json Xml

Similar Datasets

Cdk8, Cyclin C, Med12 or Med13 depletion effect on gene expression in Drosophila S2 cells

Project description:Expression profiling following depletion of Mediator Cdk8 module subunits Cdk8, Cyclin C (CycC), Med12 and Med13 72 hours after dsRNA treatment of Drosophila melanogaster S2 cells. Results provide insight into the role of individual Cdk8 module subunits in regulation of transcription. 22 samples. 2 Cdk8 dsRNA, 4 CycC dsRNA, 4 Med12 dsRNA, 4 Med13 dsRNA, 8 control samples including 4 Luciferase (Luc) dsRNA and 4 GFP dsRNA

2014-04-29 | E-GEOD-52343 | biostudies-arrayexpress

Identification of Drosophila salivary gland secreted proteins through LC-MS/MS

Project description:As we observed that salivary gland ablation induced retardation of systemic growth, it raised the possibility that salivary glands might secrete a growth factor-like peptide into the hemolymph to regulate systemic growth. To identify potential salivary gland-derived peptides with endocrine activity, we performed liquid chromatography-tandem mass spectrometry (LC-MS/MS) analysis and investigated the changes in the hemolymph proteome following salivary gland ablation.

2021-11-25 | PXD026372 | Pride

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

Cdk8, Cyclin C, Med12 or Med13 depletion effect on gene expression in Drosophila S2 cells

2014-04-29 | GSE52343 | 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

Distinct effects of CDK8 module subunits on cellular growth and proliferation in Drosophila

Project description:The Mediator complex plays a pivotal role in facilitating RNA polymerase II-dependent transcription in eukaryotes. Within this complex, the CDK8 kinase module (CKM), comprising CDK8, Cyclin C (CycC), Med12, and Med13, serves as a dissociable subcomplex that modulates the activity of the small Mediator complex. Genetic studies in Drosophila have revealed distinct phenotypes associated with mutations in CKM subunits, yet the underlying mechanism has remained unknown. Using Drosophila as a model, we generated transgenic strains to individually or simultaneously deplete the four CKM subunits in all possible combinations, uncovering unique phenotypes in the eyes and wings. Depletion of CDK8-CycC enhanced E2F1 target gene expression and promoted cell-cycle progression, whereas Med12-Med13 depletion had no significant impact on these processes. Conversely, depleting Med12-Med13 altered the expression of ribosomal protein genes and fibrillarin, reduced nascent protein synthesis, indicating a severe reduction in ribosome biogenesis and cellular growth compared to the loss of CDK8-CycC. These findings reveal distinct in vivo roles for CKM subunits, with Med12-Med13 disruption having a more pronounced effect on ribosome biogenesis and protein synthesis .

2024-11-20 | GSE275182 | GEO

Cdk8 attenuates lipogenesis by inhibiting SREBP-dependent transcription in Drosophila

Project description:Fine-tuning of lipogenic gene expression is important for the maintenance of long-term homeostasis of intracellular lipids. The SREBP family of transcription factors are master regulators that control the transcription of lipogenic and cholesterogenic genes, but the mechanisms modulating SREBP-dependent transcription are still not fully understood. We previously reported that CDK8, a subunit of the transcription co-factor Mediator complex, phosphorylates SREBP at a conserved threonine residue. Here, using Drosophila as a model system, we observed that the phosphodeficient SREBP proteins (SREBP-Thr390Ala) were more stable and more potent in stimulating the expression of lipogenic genes and promoting lipogenesis in vivo than wild-type SREBP. In addition, starvation blocked the effects of wild-type SREBP-induced lipogenic gene transcription, whereas phosphodeficient SREBP was resistant to this effect. Furthermore, our biochemical analyses identified six highly conserved amino acid residues in the N-terminus disordered region of SREBP that are required for its interactions with both Cdk8 and the MED15 subunit of the small Mediator complex. These results support that the concerted actions of Cdk8 and MED15 are essential for the tight regulation of SREBP-dependent transcription.

2022-11-09 | GSE217104 | GEO

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

GeneChip Expression Array

Project description:GeneChip Expression Array

| PRJNA606964 | ENA

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

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