Browse
Submit Data
Databases
API
Help

Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

9 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

RNA-seq of Control and NCoR1 KD CD8α+ DCs at 0hr and 6hr of stimulation

ABSTRACT: RNA-seq was performed to understand the role of NCoR1 in CD8α+ DCs. MutuDC cell line was transduced with empty and Ncor1 shrna lentiviral particles and cells were prepared in unstimulated, 2hr and 6hr (IFNg, pIC and CpG+pIC+IFNg) stimulation condition.

INSTRUMENT(S): NextSeq 550

ORGANISM(S): Mus musculus

SUBMITTER: Sunil Kumar Raghav

PROVIDER: E-MTAB-10989 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

ACCESS DATA

Json Xml

Publications

Epigenomics of conventional type-I dendritic cells depicted preferential control of TLR9 versus TLR3 response by NCoR1 through differential IRF3 activation.

Mishra Gyan Prakash GP Jha Atimukta A Ahad Abdul A Sen Kaushik K Sen Aishwarya A Podder Sreeparna S Prusty Subhasish S Biswas Viplov Kumar VK Gupta Bhawna B Raghav Sunil Kumar SK

Cellular and molecular life sciences : CMLS 20220718 8

Tight control of gene regulation in dendritic cells (DCs) is important to mount pathogen specific immune responses. Apart from transcription factor binding, dynamic regulation of enhancer activity through global transcriptional repressors like Nuclear Receptor Co-repressor 1 (NCoR1) plays a major role in fine-tuning of DC responses. However, how NCoR1 regulates enhancer activity and gene expression in individual or multiple Toll-like receptor (TLR) activation in DCs is largely unknown. In this s ...[more]

PMID: 35849243

Similar Datasets

Melanoma SK-Mel-103 cell line : control vs. treated with pIC/pIC+PEI

Project description:Transcriptional profiling of the melanoma SK-mel-103 comparing control untreated cells with cells treated with 1ug/ml of polyinosine-polycytidylic acid (pIC) or 1ug/ml of pIC with polyethyleneimine (PEI) for 4 or 10 hours. Keywords: Treatment Four-condition experiment, SK-Mel-103 untreated vs. SK-Mel-103 treated with pIC/pIC+PEI at 4 and 10 hours. One replicate per array.

2010-04-08 | E-GEOD-14445 | biostudies-arrayexpress

IFNg+ vs IFNg- Treg

Project description:Gene expression studies comparing IFNg+ Tregs versus IFNg- Tregs from human peripheral blood Ex vivo sorted Tregs (CD25highCD127neg) were stimulated for 4 hours and IFNg-secreting cells were detected by a IFNg-capture kit. The samples were resorted based on IFNg expression.

2016-07-01 | E-GEOD-71274 | biostudies-arrayexpress

3’-Seq sHSC/pHSC

Project description:Here, we present a 3’-Seq dataset of ex vivo isolated mouse multipotent steady state hematopoietic stem cells (sHSC) and proliferating HSCs (16h pIC; pHSC)

2020-03-30 | E-MTAB-7390 | biostudies-arrayexpress

Identification of different human CD8 T cell subsets by superior cytotoxicity in human T cells

Project description:Cytotoxic CD8+ T cells can effectively kill target cells by producing cytokines, chemokines and granzymes. Expression of these effector molecules is however highly divergent, and tools that identify and pre-select potent killer cells are lacking. Human CD8+ T cells can be divided into IFNGand IL-2 producing cells. Unbiased RNA-sequencing and proteomics analysis on cytokine-producing fixed CD8+ T cells revealed that IL-2+ T cells produce helper cytokines, and that IFNG+ T cells produce cytotoxic molecules. IFNG+ cytotoxic T cells expressed the surface marker CD29 already prior to stimulation. CD29 also marked T cells with cytotoxic gene expression from different tissues in single-cell RNA-sequencing data. Notably, the cytotoxic features of CD29+ T cells were maintained during cell culture, suggesting a stable phenotype. Pre-selecting CD29-expressing MART1 TCR-engineered T cells potentiated the killing of target cells. We therefore propose that selecting for CD29+ T cells could boost the anti-tumoral activity of T cell therapeutics.

2021-09-08 | PXD012874 | Pride

Expression data from RAW 264.7 macrophage

Project description:IFNg is a pro-inflammatory and pro-atherogenic cytokine that leads to macrophage activation. Adenosine has well-documented anti-inflammatory properties. We used microarrays to compare the global gene expression profile in mouse macrophages stimulated with IFNg alone and those cells treated with IFNg and adenosine. We determined that adenosine suppressed the expression of many IFNg-regulated pro-inflammatory cytokines, chemokines, and other pro-atherogenic genes. Keywords: treatment response RAW 264.7 cells were treated for 4 hours with either IFNg or IFNg plus adenosine. Following treatment, total RNA was extracted and treatment groups were pooled from 2 separate experiments for hybridization of Affymetrix microarrays.

2009-12-30 | E-GEOD-14612 | biostudies-arrayexpress

Human IFNG+/- Treg and Tconv transcriptome

Project description:Microarray used to detail the global gene transcription underlying sorted IFNg+ and IFNg- Tregs (CD4+CD25+CD127lo) and Tconv (CD4+CD25-CD127+) for fresh (unexpanded) and 14 day expanded cells from human blood. Treg and Tconv were FACS isolated from five healthy subjects (median age of 26, range 22-30). Sorted cells were separated into two groups: the first group was stimulated for 4 hours with PMA/ionomycin and labeled with the IFNg cytokine capture kit (Miltenyi Biotech) followed by FACS isolation of IFNg- and IFNg+ populations. The second set was expanded to day 14 prior to reactivation and cytokine cell capture. For each IFNg sorted population, cells were pelleted and flash frozen before RNA isolation and processing.

2015-05-01 | E-GEOD-59786 | biostudies-arrayexpress

NRROS negatively regulates ROS in phagocytes during host defense and autoimmunity

Project description:Production of reactive oxygen species (ROS) is one of the important antimicrobial mechanisms of phagocytic cells. Enhanced oxidative burst requires these cells to be primed with agents such as IFNg and LPS with a synergistic effect of these agents on the level of the burst. However, excessive ROS generation will lead to tissue damage and has been implicated in a variety of inflammatory and autoimmune disease. Therefore, this process needs to be tightly regulated. In order to understand the genes regulating this process, we will treat bone marrow derived macrophages with above mentioned priming agents and study the gene expression. We used microarrays to determine the changes in gene expression that occur in bone marrow derived macrophages after treatment with IFNg, LPS, or a combination of IFNg and LPS. Four condition experiment; Biological replicates: four replicates per condition

2014-03-31 | E-GEOD-53986 | biostudies-arrayexpress

Nuclear Receptor Co-repressor NCoR1 governs immune-tolerance in conventional dendritic cells by fine-tuning glycolysis and fatty acid oxidation

Project description:In this study, we focused on demonstrating the metabolic aspect of NCoR1 in the regulation of dendritic cells (DCs) functionality. We report that NCoR1 deficient tolerogenic DCs meet their anabolic requirements through enhanced glycolysis and OxPhos, supported by FAO-driven oxygen consumption. Furthermore, individual and dual inhibition of glycolysis through HIF-1α inhibitor (KC7F2) and fatty acid oxidation through CPT1 inhibitor (etomoxir) significantly impaired the secretion of tolerogenic cytokines. To validate the same at the global mRNA level we did bulk RNA-seq to determine the differentially expressed genes in control and NCoR1 KD 6h CpG activated DCs with and without inhibitor treatment.

2024-01-01 | E-MTAB-12066 | biostudies-arrayexpress

Expression data from CD71+ cells from the bone marrow of WT, CD70TG, IFNg-/- and CD70TG*IFNg-/- mice.

Project description:CD70TG mice are a model for sterile chronic immune activation and develop Anemia of Inflammation, which is dependent on the production of Ifng by effector CD4 and CD8 T cells. We used microarrays to identify Ifng-dependent differentially expressed genes that could account for the erythropoietic defect. CD71+ cells were MACS-enriched from the bone marrow of WT, CD70TG, IFNg-/- and CD70TG*IFNg-/- male mice of 10-12 weeks of age (3 mice per genotype group).

2011-07-31 | E-GEOD-22656 | biostudies-arrayexpress

Whole transcriptome profiling of the steady state and Hh-treated (8 hrs) Alpk1+/- (heterozygous) and Alpk1-/- (knockout) BMDMs using RNA-Sequencing approach

Project description:Alpk1-deficient mice demonstrate exacerbated colitis and increased IL-12/Th1 response upon challenge with an intestinal pathobiont, Helicobacter hepaticus (Hh). Hematopoietic compartment is driving the pathogenic phenotype in this animal model, and Alpk1 is highly expressed in myeloid cells (macrophages and dendritic cells). Alpk1 deficiency has a recessive phenotype, since Alpk1+/- (heterozygous) mice show the same phenotype as the wild type mice. Mouse bone-marrow derived macrophages (BMDMs) show elevated IL-12 production in Alpk1-/- mice in response to stimulation with Hh. Since the molecular mechanism of how Alpk1 deficiency affects macrophage response to Hh is unknown, we aimed to characterise global changes in gene expression in Alpk1+/- vs Alpk1-/- bone-marrow differentiated cells (BMDMs). Cells were isolated from bone marrow of Alpk1+/- and Alpk1-/- (mixture of bone marrows from three mice per genotype) and plated in BMDM differentiation medium (RPMI, 10% FCS, penicillin and streptomycin, 50 micro beta-mercapthoethanol, 20 ng/ml recombinant mouse GM-CSF(Peprotech)), 7 million cells in per 10 sm uncoated TC dish in 10 ml of medium for eight days, extra 10 ml of medium was added to plates at day 4, before collection and replating in 96-well plates, 150 thousand cells/200 microliters of differentiation medium per well in technical triplicates per genotype/stimulation condition (R1-R3 labels of the samples). The following day BMDMs were stimulated with MOI of 10 of Hh and 10ng/ml of mouse IFNg (Peprotech) (Alpk1+/- BMDMs – het _Hh_8h vs Alpk1-/- BMDMs – alpk1_Hh_8h) or IFNg only (het _nonstim_8h vs alpk1_nonstim_8h) before lysis for RNA extraction using Quick-RNA kit from Zymo Research. Purified RNA was submitted to the Welcome Trust Centre for Human Genetics (Oxford) for RNA-Sequencing

2018-07-30 | E-MTAB-7076 | 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