Browse
Submit Data
Databases
API
Help

Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

31 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Expression data from dsDNA-stimulated mouse embryonic fibroblasts

ABSTRACT: Transfection of dsDNA into many mammalian cell types indues the production of type I interferons and interferon-stimulated genes. We performed an siRNA screen to identify genes involved in this innate immune response, and identified Abcf1. We used microarrays to determine which genes are regulated by ABCF1 following dsDNA stimulation. We treated p53-/- mouse embryonic fibroblasts (MEFs) with siRNAs targeting Abcf1 or Irf3 (positive control) or a negative control siRNA (siCtrl), and then stimulated the cells with 45-base pair dsDNA for 6 hrs or left the cells unstimulated. We then lysed the cells and hybridized the RNA to Affymetrix microarrays.

ORGANISM(S): Mus musculus

SUBMITTER: Mark Lee

PROVIDER: E-GEOD-42803 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

ACCESS DATA

Json Xml

Similar Datasets

Expression data from dsDNA-stimulated mouse embryonic fibroblasts

Project description:Transfection of dsDNA into many mammalian cell types indues the production of type I interferons and interferon-stimulated genes. We performed an siRNA screen to identify genes involved in this innate immune response, and identified Abcf1. We used microarrays to determine which genes are regulated by ABCF1 following dsDNA stimulation.

2012-12-08 | GSE42803 | GEO

Expression data from IFNbeta-stimulated 293T cells

Project description:We used microarrays to determine which genes are upregulated by IFNbeta stimulation in 293T cells. We treated 293T cells with recombinant IFNbeta for 12 hrs or left the cells unstimulated. We then lysed the cells and hybridized the RNA to Affymetrix microarrays.

2012-12-08 | E-GEOD-42802 | biostudies-arrayexpress

Genome-wide gene expression analysis of FAF1 silencing in HeLa cells

Project description:This study is designed to examine the cellular functions of human Fas-associated factor 1 (FAF1) containing multiple ubiquitin-related domains. Microarray analyses revealed that interferon stimulated genes related to antiviral response are significantly increased in FAF1 knocked down HeLa cells. Silencing FAF1 enhanced the poly I:C and respiratory syncytial virus (RSV) induced productions of type I interferons (IFNs), the target gene of interferon regulator factor 3 (IRF3). IRF3 is a key transcription factor in IFNβ signaling responsible for host innate immune response. This study also found that FAF1 and IRF3 physically associate with IPO5/importin-β3 and that overexpression of FAF1 reduces the interaction between IRF3 and IPO5/importin-β3. These findings suggest that FAF1 negatively regulates IRF3-mediated IFNβ production and antiviral innate immune response via regulating nuclear translocation of IRF3. We conclude that FAF1 plays a novel role negatively regulating virus-induced IFNβ production and antiviral response by inhibiting the translocation of active phosphorylated IRF3 from cytosol to nucleus.

2016-01-29 | GSE71665 | GEO

Transcriptomic analysis of BNC2 regulated genes in LX2 cells

Project description:Human myofibroblastic LX2 cells were transfected using a siRNA directed against BNC2 (siBNC2) or a control siRNA (siCTRL) and RNA were processed for microarray analyses.

2022-08-07 | GSE185526 | GEO

Transcriptomic analysis of BNC2 regulated genes in mouse EMS404 cells

Project description:Mouse myofibroblastic EMS404 cells were transfected using a siRNA directed against BNC2 (siBNC2) or a control siRNA (siCTRL) and RNA were processed for microarray analyses.

2022-08-07 | GSE199626 | GEO

Estrogen-dependent gene expression in human breast cancer cells relies upon proteosome-dependent monoubiquitination of histone H2B

Project description:The estrogen receptor-alpha (ERÎ±) determines breast cancer cell phenotype and is a prognostic indicator. A better understanding of the mechanisms controlling ERÎ± function may uncover improved strategies for the treatment of breast cancer. Proteasome inhibition was previously reported to regulate estrogen-induced transcription but the mechanisms by which it influences ERÎ± function remain controversial. In this study we investigated the transcriptome-wide effects of the proteasome inhibitor Velcade on estrogen-regulated transcription in MCF7 human breast cancer cells and demonstrate a specific global decrease in estrogen-induced transcription. This set contains 21 microarray samples. 3 controls, 3 estrogen stimulated, 3 Bortezomib + estrogen stimulated, 2* 3 siRNA controls, 3 siRNA PSMB3 knockdowns, 3 siRNA PSMB5 knockdowns

2011-11-22 | E-GEOD-31118 | biostudies-arrayexpress

Genome-wide binding of transcription factor IRF3

Project description:Genome-wide binding of IRF3 was analysed in MM1.S cells using ChIP-seq high-throughput approach. MM1.S cells were fixed in 1% formaldehyde (Alfa Aesar) for 15min at room temperature. cells were lysed with hypotonic lysis buffer for 15minutes followed by nuclear lysis buffer for 15min on ice. ChIP for IRF3 performed by a standard ChIP-seq protocol and the genome-wide binding of IRF3 data was analysed which revealed peaks enrichment at cell cycle genes TSS.

2021-02-28 | GSE163481 | GEO

Identification of STAT3 downstream targets involved in chemoradiotherapy resistance

Project description:RNA-Seq data of human colorectal cancer cell line SW837 transfected with siRNA against STAT3 (siSTAT3) or control RNA (siCtrl), untreated or treated with Hyper-IL-6 (Hy-IL-6)

2021-01-25 | GSE139455 | GEO

The role of unliganded thyroid hormone receptors (TRs) in human adipose derived stem cells (hADSC)

Project description:Analysis of change in transcriptosome after TRÎ± or TRÎ² knockdown in hADSC. Analysis of effects of siRNA transfection (siCtrl, siTRÎ±, siTRÎ² or siETV5) in hADSC at gene expression level.The hypothesis tested in the present study was that unliganded TRÎ± and TRÎ² have distinctive roles in these cells. Total RNA was obtained from hADSC, transfected with siCtrl, siTRÎ±, siTRÎ² or ETV5. siTRÎ±, siTRÎ² or siETV5 samples were compared to siCtrl samples.

2016-10-26 | E-GEOD-75692 | biostudies-arrayexpress

IRF3 and type I interferons fuel a fatal response to myocardial infarction [single cell RNA-Seq]

Project description:Interferon regulatory factor 3 (IRF3) and type I interferons (IFNs) protect against infections1 and cancer2, but excessive IRF3 activation and type I IFN production cause autoinflammatory conditions such as Aicardi?Goutières syndrome3,4 and STING-associated vasculopathy of infancy (SAVI)3. Myocardial infarction (MI) elicits inflammation5, but the dominant molecular drivers of MI-associated inflammation remain unclear. Here we show that ischemic cell death and uptake of cell debris by macrophages in the heart fuel a fatal response to MI by activating IRF3 and type I IFN production. In mice, single-cell RNA-seq analysis of 4,215 leukocytes isolated from infarcted and non-infarcted hearts showed that MI provokes activation of an IRF3?interferon axis in a distinct population of interferon-inducible cells (IFNICs) that were classified as cardiac macrophages. Mice genetically deficient in cyclic GMP-AMP synthase (cGAS), its adaptor STING, IRF3, or the type I IFN receptor IFNAR exhibited impaired interferon-stimulated gene (ISG) expression and, in the case of mice deficient in IRF3 or IFNAR, improved survival after MI as compared to controls. Interruption of IRF3-dependent signaling resulted in decreased cardiac expression of inflammatory cytokines and chemokines and decreased inflammatory cell infiltration of the heart, as well as in attenuated ventricular dilation and improved cardiac function. Similarly, treatment of mice with an IFNAR-neutralizing antibody after MI ablated the interferon response and improved left ventricular dysfunction and survival. These results identify IRF3 and the type I IFN response as a potential therapeutic target for post-MI cardioprotection.

2017-11-06 | GSE106472 | 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