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ChIP-seq analysis to understand the mechanistic role of NCoR1 as a tolerogenic program suppressor in dendritic cells

ABSTRACT: ChIP-seq analysis to understand the mechanistic role of NCoR1 as a tolerogenic program suppressor in dendritic cells

PROVIDER: PRJNA433709 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR6704010.fastq.gz	Fastqsanger.gz
	SRR6704012.fastq.gz	Fastqsanger.gz
	SRR6704016.fastq.gz	Fastqsanger.gz
	SRR6704018.fastq.gz	Fastqsanger.gz
	SRR6704009.fastq.gz	Fastqsanger.gz

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ChIP-seq analysis to understand the mechanistic role of NCoR1 as a tolerogenic program suppressor in dendritic cells

Project description:We found in our study that NCoR1 knock down dendritic cells (DCs) develop tolerogenic behavior upon activation and these cells have the potential to modulate T helper cell differentiation toward Treg phenotype. Here to understand the mechanism of this process we performed NCoR1 ChIP-seq in wild type DCs before and after CpG ligand activation and transcriptome analysis of NCoR1 KD DCs to identify the direct and indirect target genes. We also predicted PU.1 as the recruting factor for NCoR1 in DCs based on motif enrichment and later on validated that by performing PU.1 ChIP-seq in control and NCoR1 KD DCs.

2019-10-18 | GSE110421 | GEO

RNA-seq and ChIP-seq analysis to understand the mechanistic role of NCoR1 as a tolerogenic program suppressor in dendritic cells

Project description:RNA-seq and ChIP-seq analysis to understand the mechanistic role of NCoR1 as a tolerogenic program suppressor in dendritic cells

| PRJNA433674 | ENA

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

RNA-seq and ChIP-seq analysis to understand the mechanistic role of NCoR1 as a tolerogenic program suppressor in dendritic cells

Project description:This SuperSeries is composed of the SubSeries listed below.

2019-10-18 | GSE110423 | GEO

Next Generation Sequencing Facilitates Quantitative Analysis of Wild Type and NCoR1 KD CD8a+ Dendritic cells with and without CpG stimulation

Project description:Purpose: The goals of this study to dissect mechanism by which NCoR1 regulate expression of diiferent genes at transcriptional level in CD8a+ Dendritic cells. Methods: mRNA expression of Control(Empty) and knockdown (NCoR1+/−) before and after CpG and pIC activation were generated by deep sequencing, in duplicate, using Illumina NextSeq 500 . The sequence reads that passed quality filters were analyzed at the transcript level with two methods:TopHat followed by Cufflinks. Results: we mapped raw reads to the mouse genome (build mm10) with TopHat. Differential expression study was carried out using Cufflinks v2.2.1 and list were filtered using fold change cut-off of 2 and q value <0.05. Conclusions: We found in our study that NCoR1 knock down dendritic cells (DCs) develop tolerogenic behavior upon activation and these cells have the potential to modulate T helper cell differentiation toward Treg phenotype. Here to understand the mechanism of this process we performed NCoR1 ChIP-seq in wild type DCs before and after CpG ligand activation and transcriptome analysis of NCoR1 KD DCs to identify the direct and indirect target genes. We also predicted PU.1 as the recruting factor for NCoR1 in DCs based on motif enrichment and later on validated that by performing PU.1 ChIP-seq in control and NCoR1 KD DCs.

2019-10-18 | GSE110422 | GEO

Gene expression analysis of Ncor1 muscle-specific knockout and PGC-1alpha muscle-specific transgenic skeletal muscle

Project description:In the present study we have studied the mechanistic and functional aspects of NCoR1 function in mouse skeletal muscle. NCoR1 muscle-specific knockout mice exhibited an increased oxidative metabolism. Global gene expression analysis revealed a high overlap between the effects of NCoR1 deletion and peroxisome proliferator-activated receptor (PPAR) gamma coactivator 1alpha (PGC-1alpha) overexpression on oxidative metabolism in skeletal muscle. The repressive effect of NCoR1 on oxidative phosphorylation gene expression specifically antagonizes PGC-1alpha-mediated coactivation of ERRalpha. We therefore delineated the molecular mechanism by which a transcriptional network controlled by corepressor and coactivator proteins determines the metabolic properties of skeletal muscle, thus representing a potential therapeutic target for metabolic diseases. Gene expression of a total of 20 gastrocnemius samples from control (CON, n = 5), NCoR1 muscle-specific knockout (NCoR1 MKO, n = 5), wild type (WT, n = 5) and PGC-1alpha muscle-specific transgenic (PGC-1alpha mTg, n = 5) adult male mice was analyzed using GeneChipÂ® Gene 1.0 ST Array System (Affymetrix). NCoR1 MKO and PGC-1alpha mTg samples were compared to CON and WT samples, respectively.

2013-01-08 | E-GEOD-40439 | 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

Breast cancer plasticity is restrictedby a LATS1-NCOR1 repressive axis [MARS-seq]

Project description:The tumor suppressor LATS1, whose expression is often downregulated in human breast cancer, helps maintain luminal breast cancer cell identity by keeping basal-specific genes in a closed chromatin state, preventing their spurious activation. This is achieved via interaction of LATS1 with the NCOR1 nuclear corepressor and recruitment of HDAC1,driving histone H3K27 deacetylation near NCOR1-repressed “basal” genes. Consequently, decreased expression of LATS1 elevates the expression of such “basal” genes and promotes luminal-to-basal slippage.

2022-10-19 | GSE195715 | GEO

Breast cancer plasticity is restrictedby a LATS1-NCOR1 repressive axis [ATAC-seq]

2022-10-19 | GSE195714 | GEO

Gene expression analysis of Ncor1 muscle-specific knockout and PGC-1alpha muscle-specific transgenic skeletal muscle

2013-01-08 | GSE40439 | GEO