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Genome wide mapping of NFAT1 binding sites in dendritic cells and of chromatin state in steady and dectin-1 activated dendritic cell line D1

ABSTRACT: We generated genome-wide chromatin-state maps of mouse dendritic cells in steady and dectin-1 activated with or without NFAT inhibitor FK506. We found the differential H3K4me3 signatures in these cells. This study provides the epigenetic signatures of steady, dectin-1activated with or without NFAT inhibition. We also generated stable dendritic cell line D1 expressing a V5 tagging NFAT1. This cell line was used to map the global binding sites of NFAT1 upon dectin-1 activation with 10ug/ml curdlan for 30 minutes.

ORGANISM(S): Mus musculus

PROVIDER: GSE59998 | GEO | 2015/01/05

SECONDARY ACCESSION(S): PRJNA257249

REPOSITORIES: GEO

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Genome wide mapping of NFAT1 binding sites in dendritic cells and of chromatin state in steady and dectin-1 activated dendritic cell line D1

Project description:We generated genome-wide chromatin-state maps of mouse dendritic cells in steady and dectin-1 activated with or without NFAT inhibitor FK506. We found the differential H3K4me3 signatures in these cells. This study provides the epigenetic signatures of steady, dectin-1activated with or without NFAT inhibition. We also generated stable dendritic cell line D1 expressing a V5 tagging NFAT1. This cell line was used to map the global binding sites of NFAT1 upon dectin-1 activation with 10ug/ml curdlan for 30 minutes. examine NFAT1-v5 genome wide binding sites and differential H3K4me3 epigenetic modification in steady, dectinn-1 activated with or without NFAT inhibiton.

2015-01-05 | E-GEOD-59998 | biostudies-arrayexpress

Gene expression profiling of dectin-1 and NFAT responsive genes in dendritic cells

Project description:This study provides the dectin-1 and NFAT responsive genes for 2h and 4h of curdlan treatment. Affymetrix Mouse Gene 1.0ST Arrays were used to profile gene expression in curdlan-stimulated D1 cells (2h or 4h exposure) that had been treated or not with FK506 for the duration of culture. Dendritic cell line D1 was treated with curdlan for 2h and 4h, and curdlan + Fk506 for 2h and 4h in three replicate.

2015-02-04 | E-GEOD-59896 | biostudies-arrayexpress

Gene expression profiling of dectin-1 and NFAT responsive genes in dendritic cells

2015-02-04 | GSE59896 | GEO

Time course experiment of dendritic cells exposed to curdlan

Project description:Human monocyte derived dendritic cells were exposed to the pure Dectin-1 agonist Curdlan to analyze the early transcriptional activation of DCs. This experiment is related to E-MTAB-750.

2012-08-28 | E-MTAB-1213 | biostudies-arrayexpress

Dectin-1-mediated signaling leads to characteristic gene expressions in rat mast cells

Project description:Rat mast cell line RBL-2H3 was analyzed to investigate the molecular mechanism of Dectin-1-mediated activation and responses of mast cells. Dectin-1-mediated signaling stimulated characteristic gene expression, such as MCP-1, IL-4, IL-13, TNF-αand Nfkbiz. RBL-2H3 cell line stably expressing Dectin-1 was established. Non-stimulated cells (control) compared to Dectin-1-stimulated (Curdlan) cells in order to comfirm Dectin-1-mediated signaling-inducible genes. Dectin-1-stimulated cells compared to Syk inhibitor R406-pretreated cells in order to examine the importance of Syk for Dectin-1-mediated gene up-regulations.

2014-03-27 | E-GEOD-56246 | biostudies-arrayexpress

Genome-wide analysis of the CARD9/Dectin-1 transcriptional program in neutrophils and macrophages by RNA-seq

Project description:Purpose: To characterize Card9-dependent and Card9-independent Dectin-1 mediated gene expression changes in neutrophils and to compare response to Dectin-1 stimulation in neutrophils and macrophages. Method: BM neutrophils from WT and Card9-/- mice were isolated by MACS column purification and treated with or without the Dectin-1 agonist, curdlan for 3 hrs. WT BM-derived macrophages were also treated with or without curdlan for 3hrs before sample collection. Results: We identified both Card9-dependent and Card9-independent gene expression changes with Dectin-1 stimulation in neutrophils. We also identified cell-type specific differences in the response to Dectin-1 stimulation in neutrophils and macrophages. Conclusions: Dectin-1 stimulation induces significant gene expression changes regulated by either canonical Card9-dependent or non-canonical Card9-independent mechanisms.

2021-02-26 | GSE148850 | GEO

Transcription factor NFAT1 regulates systemic autoimmunity through modulation of dendritic cell property

Project description:To characterize the roles of NFAT1 in the pathogenesis of autoimmune myasthenia gravis (MG) at a genome-wide scale, we performed gene expression microarray analysis for wild-type (WT) and NFAT1 KO bone marrow-derived dendritic cells (BMDCs) with or without 2h and 12h-stimulation with pam3CSK4.

2017-07-31 | GSE92593 | GEO

Transcription profiling of mouse MyD88-deficient bone marrow-derived macrophages treated with Zymosan

Project description:Innate immune pattern recognition receptors play critical roles in pathogen detection and initiation of antimicrobial responses. We and others have previously demonstrated the importance of the beta-glucan receptor Dectin-1 in the recognition of pathogenic fungi by macrophages and dendritic cells, and have elucidated some of the mechanisms by which Dectin-1 signals to coordinate the antifungal response. While Dectin-1 signals alone are sufficient to trigger phagocytosis and Src-Syk-mediated induction of antimicrobial reactive oxygen species, collaboration with Toll-like receptor (TLR)2 signaling enhances NF-kB activation and regulates cytokine production. In this study we demonstrate that Dectin-1 signaling can also directly modulate gene expression via activation of nuclear transcription of activated T cells (NFAT) transcription factors. Dectin-1 ligation by zymosan particles or live Candida albicans yeast triggers NFAT activation in macrophages and dendritic cells. Dectin-1-triggered NFAT activation plays a role in the induction of Egr2 and Egr3 transcription factors, and cyclooxygenase 2 (Cox-2). Furthermore, we show that NFAT activation regulates IL-2, IL-10 and IL-12 p70 production by zymosan-stimulated dendritic cells. These data establish NFAT activation in myeloid cells as a novel mechanism of regulation of the innate antimicrobial response. Experiment Overall Design: Bone marrow-derived macrophages deficient in MyD88 were stimulated with zymosan, and total RNA was extracted 120 minutes after stimulation for comparison to macrophages grown under the same conditions, but not stimulated.

2008-06-14 | E-GEOD-6376 | biostudies-arrayexpress

Zymosan stimulation of MyD88-deficient bone marrow-derived macrophages

2007-01-30 | GSE6376 | GEO

Dectin-1 intracellular domain determines species-specific ligand spectrum by modulating receptor sensitivity [mouse]

Project description:C-type lectin receptors (CLRs) are a large family of immunoreceptors that recognizes polysaccharides exposed on pathogens and triggers innate immune responses. However, the ligand spectrums of the whole members have not been fully understood. In this study, we found that seaweed-derived fucan activates cells expressing human Dectin-1 but not mouse Dectin-1. In fucan, low-valency β-glucan appeared to represent this activity, as the ligand activity was eliminated by the treatment of westase, a β-glucanase. Another low-valency β-glucan, laminarin, also acts as an agonist on human Dectin-1 but not for mouse Dectin-1, whereas high-valency β-glucan curdlan activated both human and mouse Dectin-1. Reciprocal mutagenesis analysis revealed that the ligand-binding domain of human Dectin-1 did not determine its unique sensitivity to low-valency β-glucan. Rather, its intracellular domain contributes to render human Dectin-1 reactive to low-valency β-glucan. Within the hDectin-1 intracellular domain, only two amino acids, Glu2 and Pro5, were sufficient to confer sensitivity on mouse Dectin-1. Conversely, the introduction of mouse-type amino acids, Lys2 and Ser5, to human Dectin-1 reduced the reactivity. These results suggest that the intracellular domain, but not the ligand binding domain, of Dectin-1 modulate their functions which determine the ligand spectrum.

2017-08-25 | GSE98825 | GEO

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