Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

RNAseq to profile IFNg response in human primary monocytes

ABSTRACT: We did transcriptome profiling for monocytes treated with or without IFNg to characterize IFNg response.

ORGANISM(S): Homo sapiens

PROVIDER: GSE84691 | GEO | 2016/09/12

SECONDARY ACCESSION(S): PRJNA330847

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

ChIPseq to profile IFNg response in human primary monocytes

Project description:We characterized the regulation of 2 histone marks by IFNg in human monocytes

2016-09-12 | GSE84690 | GEO

ChIPseq and RNAseq to profile IFNg response in human primary monocytes

Project description:ChIPseq and RNAseq to profile IFNg response in human primary monocytes

| PRJNA330842 | ENA

IFNg treatment of monocytes

Project description:IFNg treatment of monocytes

| PRJNA597901 | ENA

IFNg Regulates NAD+ Metabolism in Human Monocytes

Project description:IFNg is an essential and pleiotropic activator of monocytes, but little is known about the changes in cellular metabolism required for IFNg-induced activation. We sought to characterize and elucidate the mechanisms by which IFNg reprograms monocyte metabolism to support its immunologic activities. Monocytes from healthy controls and patients with gain-of-function mutations in STAT1 (STAT1 GOF), or loss-of-function mutations in mitochondrial complex I (Leigh syndrome) and NADPH oxidase (chronic granulomatous disease, CGD) were metabolically phenotyped. We found that IFNg increased oxygen consumption rates (OCR), indicative of reactive oxygen species generation by both mitochondria and NADPH oxidase. Transcriptional profiling of human monocyte derived macrophages revealed that this oxidative phenotype was driven by an IFNg-induced reprogramming of NAD+ metabolism, which is dependent on nicotinamide phosphoribosyltransferase (NAMPT)-mediated NAD+ salvage to generate NADH and NADPH for oxidation by mitochondrial complex I and NADPH oxidase, respectively. Monocytes from patients with STAT1 GOF demonstrated higher than normal OCR, while monocytes from Leigh syndrome and CGD patients demonstrated reduced OCR. Chemical inhibition of NAMPT completely abrogated the IFNg-induced oxygen consumption, comparable to levels observed in CGD patients. These data identify an IFNg-induced, NAMPT-dependent, NAD+ salvage pathway that is critical for IFNg activation of human monocytes.

2021-12-31 | GSE176562 | GEO

IFNg treatment of monocytes

Project description:Human peripheral blood monocytes were treated with control or with 25 ng/ml IFNg for 24 hours. RNA was collected, processed and hybridized to Affymetrix HGU133Plus2 chips.

2019-12-28 | GSE142672 | GEO

IFNg Regulates NAD+ Metabolism in Human Monocytes

Project description:IFNg Regulates NAD+ Metabolism in Human Monocytes

| PRJNA736708 | ENA

ChIPseq and RNAseq to profile IFNg response in human primary monocytes

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

2016-09-12 | GSE84692 | GEO

Emodin inhibits macrophage classical activation [Control-LPS-IFNg-Emodin]

Project description:In order to fully characterize emodin's effects on macrophage activation, peritoneal macrophages were stimulated with LPS+IFNg with or without emodin and gene expression was analyzed using a whole genome microarray. Emodin significantly attenuated the IFNg/LPS induced changes in a large percentage of responsive genes (31%) through inhibiting multiple signaling pathways. RT-qPCR was used to confirm the results in several genes associated with M1 macrophage activation including: TNF, IL6, IL1b, iNOS, MMP2, and MMP9. Three-condition, one-color experiment: Vehicle control, LPS-IFNg or LPS-IFNg-Emodin treated periferal WBC PMN samples: 4 biological replicates each.

2016-07-04 | E-GEOD-73310 | biostudies-arrayexpress

RNA-seq of non-LPS treated (N), non-tolerized (NT), and tolerized (T) IFNg-primed macrophages pretreated with or without HDAC3i

Project description:In this experiment we investigated the effect of HDAC3 inhibition on the transcriptome of IFNg-primed macrophages under different tolerization conditions. Peripheral blood mononuclear cells (PBMCs) were isolated from 3 healthy donors. PBMCs were isolated from whole blood of healthy donors using Ficoll gradient (Invitrogen). Monocytes (CD14+ cells) were positively selected from PBMCs using CD14 Microbeads according to the manufacturer’s instructions (Miltenyi Biotec). Monocytes were subsequently treated with or without 500 nM HDAC3i (ITF3100) for 30 minutes prior to overnight IFNg priming (50 ng/mL). Cells were then kept without LPS (non-LPS; N), treated with 10 ng/mL LPS once (non-tolerized; NT), or treated with LPS twice (tolerized; T; second LPS concentration: 100 ng/mL).

2020-02-12 | E-MTAB-8784 | biostudies-arrayexpress

Emodin inhibits macrophage classical activation [Control-LPS-IFNg-Emodin]

2016-01-02 | GSE73310 | GEO