Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

ChIPseq to profile IFNg response in human primary monocytes

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

ORGANISM(S): Homo sapiens

PROVIDER: GSE84690 | GEO | 2016/09/12

SECONDARY ACCESSION(S): PRJNA330846

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

RNAseq to profile IFNg response in human primary monocytes

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

2016-09-12 | GSE84691 | 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

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

IFNg Regulates NAD+ Metabolism in Human Monocytes

Project description:IFNg Regulates NAD+ Metabolism in Human Monocytes

| PRJNA736708 | ENA

Cell specific response to IFNg

Project description:Cell specific response to IFNg

| PRJNA449370 | ENA

IFNg+ vs IFNg- Treg

Project description:Gene expression studies comparing IFNg+ Tregs versus IFNg- Tregs from human peripheral blood Ex vivo sorted Tregs (CD25highCD127neg) were stimulated for 4 hours and IFNg-secreting cells were detected by a IFNg-capture kit. The samples were resorted based on IFNg expression.

2016-07-01 | E-GEOD-71274 | biostudies-arrayexpress

Identification of bivalent genes in CD14+ Monocytes

Project description:Identification of bivalent genes, marked with both H3K4me3 and H3K27me3, in CD14+ Monocytes. Used previously published data sets for histone marks GSM1003536 and GSM1003564.

2023-04-24 | GSE226811 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data