Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

The transcription factor EGR2 is the molecular linchpin connecting STAT6 activation to the stable epigenomic program of alternative macrophage polarization

ABSTRACT: The transcription factor EGR2 is the molecular linchpin connecting STAT6 activation to the stable epigenomic program of alternative macrophage polarization

PROVIDER: PRJNA634372 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR11828500.fastq.gz	Fastqsanger.gz
	SRR11828501.fastq.gz	Fastqsanger.gz
	SRR11828502.fastq.gz	Fastqsanger.gz
	SRR11828503.fastq.gz	Fastqsanger.gz
	SRR11828504.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 72

Similar Datasets

The transcription factor EGR2 is the molecular linchpin connecting STAT6 activation to the stable epigenomic program of alternative macrophage polarization

Project description:Macrophages polarize into functionally distinct subtypes while responding to microenvironmental cues. The identity of proximal transcription factors (TFs) downstream of the polarization signals are known, but their activity is typically transient, failing to explain the long-term, stable epigenomic programs developed. Here, we mapped the early and late epigenomic changes of interleukin-4 (IL-4)-induced alternative macrophage polarization. We identified the TF, Early Growth Response 2 (EGR2), bridging the early-transient and late-stable gene expression program of polarization. EGR2 is a direct target of IL-4-activated STAT6, having broad action indispensable for 77% of the induced gene signature of alternative polarization, including its autoregulation and a robust, downstream TF cascade involving PPARG. Mechanistically, EGR2 binding results in chromatin opening and the recruitment of chromatin remodelers and RNA-polymerase II. Egr2 induction is evolutionarily conserved during alternative polarization of mouse and human macrophages. In the context of tissue resident macrophages, Egr2 expression is most prominent in the lung of a variety of species. Thus, EGR2 is an example of an essential and evolutionarily conserved broad acting factor, linking transient polarization signals to stable epigenomic and transcriptional changes in macrophages.

2020-09-15 | GSE151015 | GEO

The transcription factor EGR2 is the molecular linchpin connecting STAT6 activation to the late, stable epigenomic program of alternative macrophage polarization.

Project description:Macrophages polarize into functionally distinct subtypes while responding to microenvironmental cues. The identity of proximal transcription factors (TFs) downstream from the polarization signals are known, but their activity is typically transient, failing to explain the long-term, stable epigenomic programs developed. Here, we mapped the early and late epigenomic changes of interleukin-4 (IL-4)-induced alternative macrophage polarization. We identified the TF, early growth response 2 (EGR2), bridging the early transient and late stable gene expression program of polarization. EGR2 is a direct target of IL-4-activated STAT6, having broad action indispensable for 77% of the induced gene signature of alternative polarization, including its autoregulation and a robust, downstream TF cascade involving PPARG. Mechanistically, EGR2 binding results in chromatin opening and the recruitment of chromatin remodelers and RNA polymerase II. Egr2 induction is evolutionarily conserved during alternative polarization of mouse and human macrophages. In the context of tissue resident macrophages, Egr2 expression is most prominent in the lung of a variety of species. Thus, EGR2 is an example of an essential and evolutionarily conserved broad acting factor, linking transient polarization signals to stable epigenomic and transcriptional changes in macrophages.

| S-EPMC7608752 | biostudies-literature

Genetic interrogation of STAT6-mediated macrophage polarization to tumorigenesis in a sterile, penetrant, autochthonous cancer model

Project description:Macrophage recruitment into tumors is correlated with poor outcomes in cancer, which correlate with STAT6-dependent M2 macrophage polarization and wound healing-type responses. Using penetrant, genetic models of neuroblastoma, we found macrophage recruitment was protective against tumor formation while disabling STAT6-mediated M2 polarization had no effect on tumorigenesis, progression or expression of key immunosuppressive pathways. Thus while macrophages are drivers of cancer in this model, non-classical M2 STAT6-independent pathways are plausible targets for cancer therapy.

2018-05-01 | GSE98763 | GEO

RNA-seq of FR4+Egr2+, FR4+Egr2-, FR4-Egr2-, FR4+Egr2-/-Egr3-/- and FR4-Egr2-/-Egr3-/- CD4 T cells

Project description:Transcription profiling of mouse FR4+Egr2+, FR4+Egr2- and FR4-Egr2- CD4+ T cells extracted from GFP-Egr2 knockin (Egr2 Kin) and FR4+Egr2-/-Egr3-/- and FR4-Egr2-/-Egr3-/- CD4+ T cells isolated from Egr2loxP/loxP hCD2-Cre Egr3-/- (Egr2/3 DKO) mice in the steady state or 21 days after infection with vaccinia virus.

2025-01-01 | E-MTAB-12736 | biostudies-arrayexpress

Activation of STAT6 by STING Is Critical for Antiviral Innate Immunity

Project description:Analysis of the transcriptional response of HEK293 or HEK293-STAT6 stable cell lines to poly(I:C) transfection. The hypothesis tested was that poly(I:C) transfection is capable of inducing the expression of STAT6-dependent antiviral genes. mRNA isolated from HEK293 or HEK293-STAT6 stable cell lines with control treatment or poly(I:C) transfection for 16 hours.

2011-11-21 | E-GEOD-26435 | biostudies-arrayexpress

Genome-wide detection of STAT6 binding sites in IL-4 treated naive human CD4+ T cells

Project description:STAT6 is a major transcription factor driving the polarization of Th2 cells in response to IL-4. STAT6 is phosphorylated by Jak1 and Jak3 kinases at the IL-4 receptor, after which phosphorylated STAT6 forms a homodimer and translocates into the nucleus. There STAT6 binds to specific DNA sequences, regulating the transcription of its target genes. Here we have analyzed on a genome wide level the STAT6 binding sites, after 1h and 4h of IL-4 induction, in naive human CD4+ T cells. Keywords: SRA Altogether 5 samples from 1 biological replicate were analyzed. Activated and IL-4 treated samples were compared to only activated or untreated samples to identify unique STAT6 binding sites after IL-4 induction.

2010-06-25 | E-GEOD-17850 | biostudies-arrayexpress

Frank2021 - Macrophage polarization

Project description:The model describes the mechanisms by which macrophages differentiate into a given phenotype. The model shows that both extracellular and intracellular signalling are both important for that process. More specifically, STAT1 activity favors macrophages polarization towards M1 phenotype and STAT6 activity favors macrophage polarization towards M2 phenotype. However, these polarizations are can be reversed by molecular signalling.

2024-09-02 | BIOMD0000001060 | BioModels

Genome-wide analysis of STAT6 target genes in IL-4 treated human cord blood CD4+ cells

Project description:STAT6 is a major transcription factor driving the polarization of Th2 cells in response to cytokine IL-4. Here we have analyzed on a genome wide level the STAT6 mediated gene expression after IL-4 induction in naive human CD4+ T cells. RNAi mediated STAT6 knockdown was used to reveal the genes specifically regulated by STAT6. Total RNA from STAT6 siRNA treated cord blood CD4+ T cells 12, 24, 48 or 72 hours after culturing the cells in activating (antiCD3+antiCD28) plus or minus IL-4 conditions was compared to total RNA from nonspecific control siRNA treated cells. All together 18 samples were analyzed and 3 biological replicates of the culture were performed for a total of 54 samples.

2010-07-29 | E-GEOD-17851 | biostudies-arrayexpress

RNA-seq of FR4+Egr2+, FR4+Egr2-, FR4-Egr2-, FR4+Egr2-/-Egr3-/- and FR4-Egr2-/-Egr3-/- CD4 T cells

Project description:RNA-seq of FR4+Egr2+, FR4+Egr2-, FR4-Egr2-, FR4+Egr2-/-Egr3-/- and FR4-Egr2-/-Egr3-/- CD4 T cells

| PRJEB60459 | ENA

Genome-wide analysis of STAT6 target genes in IL-4 treated human cord blood CD4+ cells

2010-06-25 | GSE17851 | GEO