Browse
Submit Data
Databases
API
Help

Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

10 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Global analysis of Cdk9-dependence for VSV-induced genes in Drosophila cells

ABSTRACT: To determine the Cdk9 targets of VSV-induced genes in Drosophila cells at 4 hours post-infection Drosophila cells were treated with Bgal or Cdk9 and infected with VSV (MOI 10) for 4 hours, in two independent biological replicates. Total RNA was isolated using Trizol and microarray experiments were performed at the University of Pennsylvania Microarray Facility (U. Penn MF) following directions according to the manufacturerM-bM-^@M-^Ys protocol (Affymetrix). In brief, 100 ng RNA were amplified with the Ovation RNA Amplification System v2 (NuGen), the Encore Biotin Module (NuGen) was used for fragmentation and labeling, Protocol FS450 002 was used for hybridization, washing, and staining. Images were scanned using the GeneChipM-BM-. Scanner 3000 and image analysis was performed using the AffymetrixM-BM-. GeneChipM-BM-. Command ConsoleM-BM-. Software (AGCC).

ORGANISM(S): Drosophila melanogaster

SUBMITTER: Sara Cherry

PROVIDER: E-GEOD-41242 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

ACCESS DATA

Json Xml

Similar Datasets

Expression data from uninfected and VSV-infected Drosophila cells at 4 hours post-infection

Project description:Expression profiling of rapidly-induced genes upon VSV infection at 4 hours post-infection in Drosophila cells Drosophila cells were treated with Bgal dsRNA and either treated as uninfected or infected with VSV (MOI 10) for 4 hours, in two independent biological replicates. Total RNA was isolated using Trizol and microarray experiments were performed at the University of Pennsylvania Microarray Facility (U. Penn MF) following directions according to the manufacturerM-bM-^@M-^Ys protocol (Affymetrix). In brief, 100 ng RNA were amplified with the Ovation RNA Amplification System v2 (NuGen), the Encore Biotin Module (NuGen) was used for fragmentation and labeling, Protocol FS450 002 was used for hybridization, washing, and staining. Images were scanned using the GeneChipM-BM-. Scanner 3000 and image analysis was performed using the AffymetrixM-BM-. GeneChipM-BM-. Command ConsoleM-BM-. Software (AGCC).

2012-10-18 | E-GEOD-41146 | biostudies-arrayexpress

Global analysis of Cdk9-dependence for VSV-induced genes in Drosophila cells

Project description:To determine the Cdk9 targets of VSV-induced genes in Drosophila cells at 4 hours post-infection

2012-10-18 | GSE41242 | GEO

Expression profiling of HeLa cell line treated with CDK9 inhibitor

Project description:CDK9 is the kinase subunit of P-TEFb that enables RNA polymerase (Pol) II to transit from promoter-proximal pausing to productive elongation. Although considerable interest exists in CDK9 as a therapeutic target, little progress has been made due to the lack of highly selective inhibitors. Here, we describe the development of i-CDK9 as such an inhibitor that potently suppresses CDK9 phosphorylation of substrates and causes genome-wide Pol II pausing. While most genes experience reduced expression, MYC and other primary response genes increase expression upon sustained i-CDK9 treatment. Essential for this increase, the bromodomain protein BRD4 captures P-TEFb from 7SK snRNP to deliver to target genes and also enhances CDK9’s activity and resistance to inhibition. Because the i-CDK9-induced MYC expression and binding to P-TEFb compensate for P-TEFb’s loss of activity, only the simultaneous inhibition of CDK9 and MYC can efficiently induce growth arrest and apoptosis of cancer cells, suggesting the potential of a combinatorial treatment strategy. We used microarrays to examine the global impact on gene expression by imhibiting CDK9 at different time durations. HeLa cell lines treated with CDK9 inhibitor at different time points

2015-06-17 | E-GEOD-60952 | biostudies-arrayexpress

Compensatory induction of MYC expression by sustained CDK9 inhibition via a BRD4-dependent mechanism: Pol II occupancy profiling by ChIP-Seq in HeLa cell line in the presence or absence of CDK9 inhibition

Project description:CDK9 is the kinase subunit of P-TEFb that enables RNA polymerase (Pol) II to transit from promoter-proximal pausing to productive elongation. Although considerable interest exists in CDK9 as a therapeutic target, little progress has been made due to the lack of highly selective inhibitors. Here, we describe the development of i-CDK9 as such an inhibitor that potently suppresses CDK9 phosphorylation of substrates and causes genome-wide Pol II pausing. While most genes experience reduced expression, MYC and other primary response genes increase expression upon sustained i-CDK9 treatment. Essential for this increase, the bromodomain protein BRD4 captures P-TEFb from 7SK snRNP to deliver to target genes and also enhances CDK9’s activity and resistance to inhibition. Because the i-CDK9-induced MYC expression and binding to P-TEFb compensate for P-TEFb’s loss of activity, only the simultaneous inhibition of CDK9 and MYC can efficiently induce growth arrest and apoptosis of cancer cells, suggesting the potential of a combinatorial treatment strategy. ChIP-seq of Pol II in HeLa cells before or after i-CDk9 treatment

2015-06-17 | E-GEOD-60953 | biostudies-arrayexpress

Influences of CDK9 on gene expressions

Project description:To understand better the contribution of CDK9 in P. gingivalis-stimulated gene expression, gene chips were performed. Lentiviral vectors carrying CDK9 shRNA or not were transfected into cells for 96 hours, with the assist of Envirus. NC group was transfected with non-targeting scramble and stimulated with PBS. NC and Pg group was transfected with non-targeting scramble and stimulated with P. gingivalis. CDK9 shRNA group was transfected with CDK9 shRNA and stimulated with PBS. CDK9 shRNA and Pg group was transfected with CDK9 shRNA and stimulated with P. gingivalis.

2019-10-11 | GSE138679 | GEO

Targeting CDK9 Reactivates Epigenetically Silenced Genes in Cancer

Project description:Cyclin-Dependent Kinase 9 (CDK9) as part of the PTEFb complex promotes transcriptional elongation by promoting RNAPII pause release. We now report that, paradoxically, CDK9 is also essential for maintaining gene silencing at heterochromatic loci. Through a live cell screen, we discovered that CDK9 inhibition reactivates epigenetically silenced genes in cancer, leading to restored tumor suppressor gene expression and cell differentiation, along with activation of endogenous retrovirus (ERV) genes. CDK9 inhibition dephosphorylates the SWI/SNF protein SMARCA4 and represses HP1α expression, both of which contribute to gene reactivation. Based on gene activation, we developed the highly selective and potent CDK9 inhibitor MC180295 (IC50 =5.1nM) that has broad anti-cancer activity in-vitro and is effective in in-vivo cancer models. Additionally, CDK9 inhibition sensitizes with the immune checkpoint inhibitor α-PD-1 in vivo, making it an excellent target for epigenetic therapy of cancer.

2020-05-26 | PXD007925 | Pride

Expression data from mouse peritoneal macrophages

Project description:Biologic functions involved in innate immune response of macrophages rely on the precise regulation of kinds of immune molecular. In the virus infection procession, the macrophages are activated following a tightly controlled genetic programme where specific sets of genes are up-regulated or down-regulated. We used microarrays to detail the global programme of gene expression underlying VSV infection and identified distinct classes of up-regulated and down-regulated genes during this process. Mouse peritoneal macrophages were selected with/without VSV infection for 8 hours for RNA extraction and hybridization on Affymetrix microarrays. We sought to obtain expression profiles. We selected macrophages according to VSV infection at two time-points: uninfected macrophage(control) and VSV infected for 8 hour macrophages(VSV).

2012-07-23 | E-GEOD-39620 | biostudies-arrayexpress

miRNA profiling of mouse primary peritoneal macrophages infected with vesicular stomatitis virus (VSV)

Project description:To investigate whether and what miRNAs expression might be regulated by VSV (vesicular stomatitis virus?) challenge, we analyzed the miRNA expression profile of mouse primary peritoneal macrophages infected with VSV by using an array-based miRNA profiling. After the infection of VSV at MOI 10 for 48 h, the array revealed that many miRNAs were up-regulated in macrophages?

2009-05-11 | E-MEXP-2110 | biostudies-arrayexpress

Identification of CDK9 targets using DRB and quantitative phosphoproteomics

Project description:CDK9 is a critical kinase required for the productive transcription of protein-coding genes by RNA polymerase II (pol II) in higher eukaryotes. Phosphorylation of targets including the elongation factor SPT5 and the carboxyl-terminal domain (CTD) of RNA pol II allow the polymerase to pass an early elongation checkpoint (EEC), which is encountered soon after initiation. In addition to halting RNA polymerase II at the EEC, CDK9 inhibition also causes premature termination of transcription across the last exon, loss of polyadenylation factors from chromatin, and loss of polyadenylation of nascent transcripts. Inhibition of the phosphatase PP2A abrogates the premature termination and loss of polyadenylation caused by CDK9 inhibition, suggesting that CDK9 and PP2A, working together, regulate the coupling of elongation and transcription termination to RNA maturation. Our phosphoproteomic analyses, using either DRB or an analog-sensitive CDK9 cell line confirm the splicing factor SF3B1 as an additional key target of this kinase. CDK9 inhibition causes loss of interaction of splicing and export factors with SF3B1, suggesting that CDK9 also helps to co-ordinates coupling of splicing and export to transcription.

2022-08-22 | PXD026720 | Pride

Expression data from C57BL/6J and C57BL6/J Sarm-deficient mice uninfected or infected with vesicular stomatitis virus (VSV)

Project description:Sarm-deficient mice are protected from VSV encephalitis and death. Microarray was done to examine genes contributing to this phenotype WT and KO mice were infected with VSV and brains were harvested at day 5 post-infection for RNA extraction

2013-04-04 | E-GEOD-44331 | 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