Browse
Submit Data
Databases
API
Help

Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

43 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Expression data from the comparison between poly(I:C)-treated WT and Oasl1-/- BMDMs

ABSTRACT: Oasl1-/- BMDMs express more type I IFN upon poly(I:C) treatment. Because OASL1 seems to rather specifically suppress the type I IFN expression, we tried to address the specificity by determining the defects associated with the Oasl1 mutation using genome-wide gene expression microarray analysis under moderate poly(I:C) stimulation (5 Âµg/ml for 9 h); this condition was used to identify the primary targets of OASL1 while minimizing the secondary targets induced by the earlier, higher production of type I IFNs in Oasl1-/- cells. Only 23 genes out of approximately 35,000 probed transcripts showed a signal difference greater than two-fold between the WT and KO cells; 15 showed higher signals in KO cells while 8 showed lower signals in KO cells We analyzed total RNA from poly(I:C)-treated WT and Oasl1-/- BMDM using the Affymetrix Mouse Gene 1.0 ST array. Array data were processed by Affymetrix GCOS software. We compared these using Affymetrix Expression console1.1, TMEV4.4, DAVID.

ORGANISM(S): Mus musculus

SUBMITTER: Byungil Kim

PROVIDER: E-GEOD-41788 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

ACCESS DATA

Json Xml

Similar Datasets

Genome-wide polysome analysis in poly(I:C)-treated WT and Oasl1-/- BMDM.

Project description:OASL1 is a novel translation inhibitor for the type I IFN master transcription factor IRF7. To examine whether OASL1 specifically inhibit IRF7 translation, we used a genome-wide gene expression microarray to screen for the polysome-associated mRNAs more enriched in the OASL1 KO BMDMs. The microarray analysis on the polysomal fractions identified 145 candidate transcripts, including IRF7, that showed a signal greater than two-fold higher in poly(I:C)-treated Oasl1-/- BMDM. We analyzed polysomal fractions from poly(I:C)-treated WT and Oasl1-/- BMDM using the Affymetrix Mouse Gene 1.0 ST array. Array data were processed by Affymetrix GCOS software. We compared these using Affymetrix Expression console1.1, R affy-package(2.9.2), DAVID.

2013-02-17 | E-GEOD-41787 | biostudies-arrayexpress

Expression data from the comparison between poly(I:C)-treated WT and Oasl1-/- BMDMs

Project description:Oasl1-/- BMDMs express more type I IFN upon poly(I:C) treatment. Because OASL1 seems to rather specifically suppress the type I IFN expression, we tried to address the specificity by determining the defects associated with the Oasl1 mutation using genome-wide gene expression microarray analysis under moderate poly(I:C) stimulation (5 µg/ml for 9 h); this condition was used to identify the primary targets of OASL1 while minimizing the secondary targets induced by the earlier, higher production of type I IFNs in Oasl1-/- cells. Only 23 genes out of approximately 35,000 probed transcripts showed a signal difference greater than two-fold between the WT and KO cells; 15 showed higher signals in KO cells while 8 showed lower signals in KO cells

2013-02-17 | GSE41788 | GEO

ZBP1 is a cytosolic RNA virus sensor driving activation of the NLRP3 inflammasome, pyroptosis, necroptosis and apoptosis

Project description:The innate immune system recognizes nucleic acids as a signature of microbial infection and initiates host-protective responses, including the production of type I IFN and proinflammatory cytokines. Z-DNA binding protein 1 (ZBP1, also known as DLM-1 or DAI) was previously identified as a dsDNA binding protein, triggering DNA-mediated activation of innate immune responses. However, mice or cells lacking ZBP1 produce normal levels of type I IFN in response to dsDNA. Therefore, the classification of ZBP1 as a true DNA sensor remains to be resolved. Here, we report that the single stranded RNA virus, influenza A virus (IAV) is a trigger of the cytosolic sensor ZBP1. Sensing of IAV infection by ZBP1 engages a novel NLRP3 inflammasome pathway that is not defined by the conventions of the canonical and non-canonical NLRP3 inflammasome pathways. Surprisingly, IAV-induced cell death was not prevented by the absence of the NLRP3 inflammasome. Instead, we identified parallel contributions from pyroptosis, necroptosis and apoptosis in the execution of ZBP1-dependent cell death, mediated by the kinase RIPK3. Overall, the ability of ZBP1 to sense IAV infection signifies a point of divergence for IAV-induced programmed cell death pathways and inflammasome activation. We used microarrays to explore the gene expression profiles differentially expressed in influenza-infected bone marrow derived macrophages (BMDM) isolated from Ifnar1-/- and wild-type mice.

2016-08-11 | E-GEOD-77611 | biostudies-arrayexpress

ChIP-seq to profile LPS-induced RNA polymerase II transcription in bone marrow-derived macrophages from WT and Hes1 KO mice

Project description:We characterized the RNA polymerase II occupancy on gene loci in WT and Hes1 KO BMDMs under untreated and LPS-stimulated conditions WT and Hes1 KO BMDMs were left untreated or stimulated with LPS for 1 hour. Pol II ChIP was performed and the DNA products were subject to ChIPseq

2016-06-13 | E-GEOD-73568 | biostudies-arrayexpress

Optimization of transcription factor binding map accuracy by utilizing their knockout-mouse models

Project description:Genome-wide assessment of protein-DNA interactions binding by ChIP-seq is a key technology to study transcription factor (TF) localization and regulation of gene-expression. In ChIP-seq, signal-to-noise-ratio as well as signal specificity depend on many variables including antibody quality, and efforts to improve ChIP-seq data thus far focused mostly on generating better reagents. Here we introduce KOIN (KO implemented normalization) as a novel strategy to increase signal specificity and reduce noise by using TF knockout-mice as a critical control for ChIP-seq. We tested our new peak calling strategy (KO implemented normalization = KOIN) on different ChIP-seq datasets to increase signal specificity and reduce noise.

2014-07-17 | E-GEOD-55317 | biostudies-arrayexpress

Gut hepcidin: a key regulator of inflammation

Project description:Hepcidin is demonstrated to be the key iron regulatory hormone, produced by the liver. Here we show an unexpected role of hepcidin as a master initiator of the local and systemic inflammatory response. We found that hepcidin was highly expressed in the colon of two major idiopathic inflammatory bowel diseases : Crohn's disease (CD) and ulcerative colitis (UC). Thanks to the generation of intestinal specific hepcidin KO mice (Hepc{delta}int), we found in a DSS-induced colitis model that hepcidin mediated the induction of key inflammatory cytokines and was protective against intestinal injury. In a model of LPS-induced acute inflammation, intestinal hepcidin expression was increased through a TLR4 dependent pathway andwas required for intestinal neutrophil infiltration and inflammation. Strikingly, intestinal hepcidin was absolutely required for the systemic production of key inflammatory cytokines (IL-6, CXCL1, TNF-alpha ...) as well as for the setting of the hypoferremia of inflammation. In a sepsis model, Hepc{delta}int mice were protected against LPS-induced mortality. Mechanistically, we showed that hepcidin was a direct neutrophil chemoattractant and a proinflammatory molecule in macrophages through a Myd88 dependent pathway. Altogether, we demonstrated that Hepcidin is a key new essential component of the immune system and may be a promising target in many inflammatory diseases. We used microarrays to detail the global program of gene expression of BMDM treat with hepcidin for 1 hour.

2016-07-16 | E-GEOD-71073 | biostudies-arrayexpress

ATF3 is a central regulator of interferon-beta and interferon-stimulated genes during the innate immune response

Project description:This study shows that in the absence of Atf3, primary mouse macrophages display significantly greater basal and PRR-inducible IFNβ expression. This regulation appears to be directly on the level of Ifnb1 transcription mediated by ATF3 binding proximal to the Ifnb1 promoter under basal condition. The ATF3 expression was demonstrated to be type I IFN-inducible in both human and mouse immune cells. A subset of 36 genes downstream of IFNAR signalling were modulated in an ATF3-dependent manner.The regulation of IFN responses by ATF3 had significant relevance on in vitro viral infection. Together these findings demonstrate that ATF3 is an important regulatory handbrake that limits the magnitude of IFN responses on multiple levels; basal Ifnb1 expression; PRR-inducible IFNβ; and the expression of specific ISGs. 12 samples

2015-09-07 | E-GEOD-61055 | biostudies-arrayexpress

The specifcity of innate immune response is enforced by repression of interferon-response elements by NFkB p50

Project description:The specific binding of transcription factors to cognate sequence elements is thought to be critical for the generation of specific gene expression programs. The transcription factors nuclear factor kB (NF-kB) and the interferon (IFN) regulatory factors (IRFs) bind to the kB site and the interferon response element (IRE), respectively, of target genes, and they are activated in macrophages after exposure to pathogens. However, how these factors produce pathogen-specific inflammatory and immune responses remains poorly understood. Combining top-down and bottom-up systems biology approaches, we have identified the NF-kB p50 homodimer (p50:p50) as a regulator of IRF responses. First, unbiased genome-wide expression analysis revealed that p50 repressed a subset of IFN-inducible genes through a previously uncharacterized subclass of guanine-rich IRE (G-IRE) sequences, which was substantiated by biochemical and structural analyses. Second, mathematical modeling predicted that p50:p50 might enforce the stimulus-specificity of composite promoters. Indeed, the production of the antiviral regulator IFN-b was rendered stimulus-specific by the binding of p50:p50 to the G-IRE–containing IFNb enhancer to suppress cytotoxic IFN signaling. Specifically, a deficiency in p50 resulted in the inappropriate production of IFN-b in response to bacterial DNA sensed by Toll-like receptor 9. This role for NF-kB p50 in enforcing the specificity of the cellular response to pathogens by binding to a previously uncharacterized subset of IRE sequences alters our understanding of how the NF-kB and IRF signaling systems cooperate to regulate antimicrobial immunity. [BMDM]: Total RNA extracted from wt, p50-/- or ifnar-/- bone marrow derived macrophages (BMDMs) were subjected to stimulation with LPS, CpG or IFNb [MEF]: Total RNA extracted from wt or p50KO primary mouse embryonic fibroblasts were subjected to stimulation with LPS or IFNb

2011-03-01 | E-GEOD-27112 | biostudies-arrayexpress

Identification of ASC-interacting proteins

Project description:To explore the spatiotemporal regulation of ASC speck formation and inflammasome activation, we infected primary WT and Asc–/– bone marrow-derived macrophages (BMDMs) with the bacterium Francisella novicida to induce AIM2 inflammasome activation and then performed ASC IP-MS to identify proteins that interacted with ASC. We compared the IP products between WT BMDMs and Asc–/– BMDMs, and found that many proteins specifically interacted with ASC.

2024-05-29 | PXD052497 | Pride

Genome-wide polysome analysis in poly(I:C)-treated WT and Oasl1-/- BMDM.

2013-02-17 | GSE41787 | GEO