Browse
Submit Data
Databases
API
Help

Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

ChIP-seq of H3K27ac in Control and NCoR1 KD CD8α+ DCs at 0hr, 2hr and 6hr of TLR stimulation

ABSTRACT: H3K27ac ChIP-seq was performed to identify active enhancers in different TLR activated control CD8α+ DCs as well as to understand the role of NCoR1 in regulating TLR specific enhacner activity using H3K27ac ChIP-seq performed in NCoR1 KD DCs. MutuDC1940 cell line were treated with TLR3 ligand poly I:C, TLR9 ligand CpG-B and combined stimulation of TLR9 , TLR3, and IFNg for 2hr and 6hr. Recombinant Anti-Histone H3 (acetyl K27) antibody was used to pull down chromatin regions having active enhacner mark in each unstimulated and stimulated condition.

INSTRUMENT(S): NextSeq 550

ORGANISM(S): Mus musculus

SUBMITTER: Sunil Kumar Raghav

PROVIDER: E-MTAB-10992 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

ACCESS DATA

Json Xml

Similar Datasets

ChIP-seq of NCoR1 in CD8α+ DCs at 6hr of stimulation

Project description:ChIP-seq of NCoR1 was performed to identify binding sites of NCoR1 in TLR dependent manner. MutuDC1940 cell line were treated with TLR3 ligand poly(I:C) and combined stimulation of TLR9 (CpG-B), TLR3, and IFNg for 6hr.

2025-12-03 | E-MTAB-10991 | biostudies-arrayexpress

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

Project description: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.

2022-09-20 | E-MTAB-10989 | 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

Identification and functional characterization of NCoR1-interacting proteins associated with mitochondrial biogenesis

Project description:This study was designed to identify putative NCoR1-interacting proteins that might regulate the mitochondrial biogenesis process. To do that, MEF cells were transiently transfected with plasmid expressing either pcDNA-GFP-FLAG (control) or pCMX-NCoR1-FLAG and subjected to co-IP and identification of interacting proteins by liquid chromatography tandem mass spectrometry (LC-MS/MS) (LTQ Velos Orbitrap).

2023-07-20 | PXD040945 | Pride

Comparison of gene expression in macrophages tolerised by different toll-like receptor ligands

Project description:To investigate the similarity of toll-like receptor tolerance in macrophages stimulated with different toll-like receptor ligands we stimulated naïve or tolerant macrophages with ligands for TLR4, TLR2, TLR3 and TLR9. The data identifies a core set of genes that are tolerised by all ligands and genes that show TLR specific patterns.

2018-05-30 | GSE81291 | GEO

UNC93B1 variants underlie TLR7-dependent autoimmunity

Project description:UNC93B1 is critical for trafficking and function of nucleic acid-sensing Toll-like receptors (TLRs) TLR3, TLR7, TLR8, and TLR9, which are essential for antiviral immunity. Overactive TLR7 signaling induced by recognition of self-nucleic acids has been implicated in systemic lupus erythematosus (SLE). Here, we report UNC93B1 variants (E92G and R336L) in four patients with early-onset SLE. Patient cells or mouse macrophages carrying the UNC93B1 variants produced high amounts of TNF-α and IL-6 and upon stimulation with TLR7/TLR8 agonist, but not with TLR3 or TLR9 agonists. E92G causes UNC93B1 protein instability and reduced interaction with TLR7, leading to selective TLR7 hyperactivation with constitutive type I IFN signaling. Thus, UNC93B1 regulates TLR subtype-specific mechanisms of ligand recognition. Our findings establish a pivotal role for UNC93B1 in TLR7-dependent autoimmunity and highlight the therapeutic potential of targeting TLR7 in SLE.

2023-12-14 | GSE250223 | GEO

NCoR1, SMRT, Polymerase II and input ChIP-Seq

Project description:ChIP-seq of mouse embryonic fibroblast-adipose like cell line 3T3-L1 to identify binding sites of NCoR1 and SMRT following induction of differentiation, and RNA Pol-II after SMRT knock down

2012-04-23 | E-MTAB-1031 | biostudies-arrayexpress

Divergent principles specifying inflammatory versus antiviral transcriptional programs in dendritic cells [ATAC-seq]

Project description:Stimulus-specific gene expression programs are enabled by enhancers, on which stimulus-regulated transcription factors (SRTFs) can land in a cell type- and stimulus-dependent manner. In this study, we identified the key features of enhancers that mediate differential responses to Toll-like receptor (TLR)-stimulation. We characterized the TLR3- and TLR9-induced programs and enhancers in CD8+ dendritic cells.The relevance of these features has been confirmed via machine learning application and by mapping SRTF-binding.

2019-07-31 | GSE106743 | GEO

Divergent principles specifying inflammatory versus antiviral transcriptional programs in dendritic cells [ChIP-seq]

2019-07-31 | GSE106730 | GEO

Divergent principles specifying inflammatory versus antiviral transcriptional programs in dendritic cells [RNA-seq]

2019-07-31 | GSE106715 | GEO