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

Off-target effects of VEGF-A regulation by shRNAs

ABSTRACT: The aim of this project was to investigate how genome-wide gene expression patterns change when the expression of VEGF-A is modulated using different lentivirally delivered shRNA molecules that are complementary to VEGF-A promoter region. To study these changes, 12 gene expression array experiments were conducted with mouse endothelial cell line (C166). The C166 cells were transduced (20% confluency, MOI 10) with lentiviral vectors that all express GFP marker gene and two of them express additional shRNA molecule that is complementary to different regions in the VEGF-A promoter and either up-regulate (VEGF-up) or downregulate (VEGF-down) VEGF-A expression. Fresh medium was changed 72h after transduction. Cells were collected at day 7.

ORGANISM(S): Mus musculus

SUBMITTER: Mikko Turunen

PROVIDER: E-GEOD-47444 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

ACCESS DATA

Json Xml

Similar Datasets

Off-target effects of VEGF-A regulation by shRNAs

Project description:The aim of this project was to investigate how genome-wide gene expression patterns change when the expression of VEGF-A is modulated using different lentivirally delivered shRNA molecules that are complementary to VEGF-A promoter region. To study these changes, 12 gene expression array experiments were conducted with mouse endothelial cell line (C166).

2015-08-06 | GSE47444 | GEO

Expression data from TSA-treated Plasmodium

Project description:Variation of surface adhesins is a critical mediator of virulence and immune evasion in many medically important microbes. Phenotypic switching has been linked to transcriptional changes and the function of chromatin proteins, but the determinants of the rate of phenotypic switching remain poorly defined. We analyzed epigenetic switching of the Plasmodium falciparum erythrocyte invasion ligand PfRh4. By introducing a prokaryotic Dam methylase, we demonstrate that parasites selected for in vivo PfRh4 activation show a reversible increase in promoter accessibility while exhibiting perinuclear repositioning of the locus from a silent to a conserved activation domain. Forced activation of a proximal gene results in a similar level of repositioning of the PfRh4 locus into this domain and a concomitant increase in PfRh4 activation in a sub-population of parasites, with promoter accessibility occurring only at actively transcribed loci. Thus, we reveal two distinct epigenetic mechanisms regulating the expression of a malaria virulence gene. To examine the correlation between changes in gene expression induced by treatment with a high dose of trichostatin A (TSA) and the associated changes in chromatin accessibility. Plasmodium falciparum was treated (or not, control) with 100nm or 500nm TSA, and then the expression profiles were analyzed.

2012-10-13 | E-GEOD-41567 | biostudies-arrayexpress

Expression data from glioblastoma cells after ZFHX4 or CHD4 suppression.

Project description:ZFHX4 and CHD4 suppression independently shift tumor initiating cells out of a stem like state and toward a differentiated morphology. After gene suppression via transduction of a lentivirally mediated shRNA construct, RNA was extracted 3 and 5 days later and was hybridized on Affymetrix microarrays. Total RNA was extracted 3 and 5 days after shRNA transduction of 0308 TICs, for 3 (for CHD4) or 5 (ZFHX4) independent experiments. Complementary RNA synthesis and hybridization/scanning of U133 plus 2.0 microarrays using GeneChip products (Affymetrix) was done as described in the GeneChip manual.

2014-01-16 | E-GEOD-52363 | biostudies-arrayexpress

Notch and VEGF pathways play distinct but complementary roles in tumor angiogenesis

Project description:We asked whether combining Notch and VEGF blockade would enhance suppression of tumor angiogenesis and growth, using the NGP neuroblastoma model. NGP tumors were engineered to express a Notch1 decoy construct (N1D), which restricts Notch signaling, and then treated with either the anti-VEGF antibody bevacizumab or vehicle. Combining Notch and VEGF blockade led to blood vessel regression, increasing endothelial cell apoptosis and disrupting pericyte coverage of endothelial cells. Combined Notch and VEGF blockade did not affect tumor weight, but did additively reduce tumor viability. Our results indicate that Notch and VEGF pathways play distinct but complementary roles in tumor angiogenesis, and show that concurrent blockade disrupts primary tumor vasculature and viability further than inhibition of either pathway alone.

2013-12-01 | GSE48880 | GEO

Transcriptomic analysis of carboxylic acid challenge in Escherichia coli: beyond membrane damage

Project description:Carboxylic acids are an attractive biorenewable chemical. Enormous progress has been made in engineering microbes for production of these compounds though titers remain lower than desired. Here we used transcriptome analysis of Escherichia coli during exogenous challenge with octanoic acid (C8) at pH 7.0. This analysis suggests that C8 challenge causes intracellular acidification and membrane damage. Escherichia coli MG1655 was grown to midlog (OD550 ~0.8) with or without 10 mM octanoic acid (pH=7.0) and the RNA was harvested and prepared for Affymetrix Microarray analysis.

2013-12-10 | E-GEOD-53140 | biostudies-arrayexpress

Notch and VEGF pathways play distinct but complementary roles in tumor angiogenesis

2013-12-01 | E-GEOD-48880 | biostudies-arrayexpress

Knock down of C11orf67 by shRNA in SUM52PE

Project description:SUM52PE cells were lentivirally transduced with PKLO empty vector control (Sigma SHC001 MISSION PLKO.1-PURO CONTROL VECTOR) or shRNA specific for C11orf67 (Sigma Clone ID: NM_024684.2-280s21c1 SHCLND-NM_024684 TRCN0000263814) in biological triplicates. Differentially regulated targets by the shRNA relative to empty vector control were determined.

2020-12-24 | GSE92893 | GEO

Human PC-3 prostate cancer cells: Control (shNTC; non-target shRNA) vs. shETV4 knock down (shETV4)

Project description:Transcriptional profiling of human PC-3 prostate cancer cells lentivirally infected with non-target control (NTC) short hairpin (sh)RNA comparing with lentivirally shRNA mediated human ETV4 knock-down. Cells were either cultured for 24 hours at 20% oxygen tension or 0.2% oxygen. Goal was to determine (i) genes affected by hypoxia in PC-3 NTC cells and (ii) identification of hypoxically induced genes requiring ETV4 for hypoxic regulation.

2011-12-06 | GSE32385 | GEO

TMEFF2 and CD95L derived shRNAs promote prostate cancer cell death by targeting the essential androgen receptor pathway

Project description:A novel mechanism, Death Induced by Survival gene Elimination (DISE), has recently been described as a potential cancer therapy. DISE kills cancer cells through an RNA interference (RNAi) mechanism. We show that expression of certain shRNAs developed to target TMEFF2 promotes prostate cancer (PCa) cell death similar to DISE, and independently of TMEFF2 targeting/expression. In PCa cells, these shRNAs downregulate the androgen receptor (AR) and AR coregulatory genes, an effect that correlates with the presence of short seed matches in their 3’UTRs and which results in global androgen signaling inhibition and cell death. We have termed this mechanism Androgen Network DISE (AN-DISE). shL3, an shRNA to CD95L known to promote DISE in non-PCa cells, promotes AN-DISE in PCa cells by targeting the AR-signaling pathway.

2021-02-01 | GSE165247 | GEO

Knockdown of Znf148 by shRNA in MDA-MB-231 breast cancer cells.

Project description:RNA-Sequencing of basal subtype triple negative breast cancer cells, MDA-MB-231. MDA-MB-231 cells were lentivirally transduced with pLKO short-hairpin (sh) luciferase control or shZnf148 in triplicates. Differentially expressed genes by the shRNA compared to the control were determined.

2022-10-04 | GSE132953 | GEO

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