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

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

PROVIDER: PRJNA433674 | ENA |

REPOSITORIES: ENA

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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

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

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

| PRJNA433709 | ENA

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

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 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

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

NCoR1 limits angiogenic capacity by altering Notch signaling [ATAC-seq]

Project description:Corepressors negatively regulate gene expression by chromatin compaction. Targeted regulation of gene expression could provide a means to control endothelial cell phenotype. We hypothesize that by targeting corepressor proteins, endothelial angiogenic function can be improved. To study this, the expression and function of nuclear corepressors in human umbilical vein endothelial cells (HUVEC) and in murine organ culture was studied. RNA-seq revealed that nuclear receptor corepressor 1 (NCoR1), Silencing Mediator of Retinoid and Thyroid hormone receptors (SMRT) and repressor element-1 silencing transcription factor (REST) are the highest expressed corepressors in HUVECs. Knockout and knockdown strategies demonstrated that the depletion of NCoR1 increased the angiogenic capacity of endothelial cells, whereas depletion of SMRT or REST did not. Interestingly, the effect was VEGF signaling independent. NCoR1 depletion significantly upregulated angiogenesis-associated genes, especially tip cell genes, including ESM1, DLL4 and NOTCH4, as observed by RNA- and ATAC-seq. Confrontation assays comparing cells with and without NCoR1-deficiency revealed that loss of NCoR1 promotes a tip-cell position during spheroid sprouting. Moreover, a proximity ligation assay identified NCoR1 as a direct binding partner of the Notch-signaling-related transcription factor RBPJk. Luciferase assays showed that siRNA-mediated knockdown of NCoR1 promotes RBPJk activity. Furthermore, NCoR1 downregulation prompts upregulation of several elements in the Notch signaling cascade. Downregulation of NOTCH4, but not NOTCH1, prevented the positive effect of NCoR1 knockdown on spheroid outgrowth. Collectively, these data indicate that decreasing NCOR1 expression is an attractive approach to promote angiogenic function.

2024-02-12 | GSE242671 | GEO

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

2013-01-08 | GSE40439 | 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

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