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Links from GEO DataSets

Items: 20

1.

IFN-γ selectively suppresses a subset of TLR4-activated genes and enhancers to potentiate M1-like macrophage polarization [ChIP-seq]

(Submitter supplied) Complete polarization of macrophages towards an M1-like proinflammatory and antimicrobial state requires combined action of IFN-γ and LPS. Synergistic activation of canonical inflammatory NF-κB target genes by IFN-γ and LPS is well appreciated, but less is known about whether IFN-γ negatively regulates components of the LPS response, and how this affects polarization. A combined transcriptomic and epigenomic approach revealed that IFN-γ selectively abrogates LPS-induced feedback and select metabolic pathways by suppressing TLR4-mediated activation of gene enhancers. more...
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL11154
21 Samples
Download data: BIGWIG
Series
Accession:
GSE120943
ID:
200120943
2.

IFN-γ selectively suppresses a subset of TLR4-activated genes and enhancers to potentiate M1-like macrophage polarization [ChIP-seq II]

(Submitter supplied) Complete activation of macrophage proinflammatory and antimicrobial phenotype is promoted by combined action of IFN-g and LPS. Synergistic activation of canonical inflammatory NF-kB target genes by IFN-g and LPS is well appreciated, but less is known about whether IFN-g negatively regulates components of the LPS response, and how this affects polarization. A combined transcriptomic and epigenomic approach revealed that IFN-g selectively abrogates LPS-induced feedback and select metabolic pathways by suppressing TLR4-mediated activation of gene enhancers. more...
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL11154
4 Samples
Download data: BIGWIG
Series
Accession:
GSE131294
ID:
200131294
3.

IFN-γ selectively suppresses a subset of TLR4-activated genes and enhancers to potentiate M1-like macrophage polarization [RNA-seq II]

(Submitter supplied) Complete polarization of macrophages towards an M1-like proinflammatory and antimicrobial state requires combined action of IFN-γ and LPS. Synergistic activation of canonical inflammatory NF-κB target genes by IFN-γ and LPS is well appreciated, but less is known about whether IFN-γ negatively regulates components of the LPS response, and how this affects polarization. A combined transcriptomic and epigenomic approach revealed that IFN-γ selectively abrogates LPS-induced feedback and select metabolic pathways by suppressing TLR4-mediated activation of gene enhancers. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL20301
24 Samples
Download data: TAB, TXT
4.

IFN-γ selectively suppresses a subset of TLR4-activated genes and enhancers to potentiate M1-like macrophage polarization

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing; Genome binding/occupancy profiling by high throughput sequencing
Platforms:
GPL11154 GPL20301
57 Samples
Download data: BIGWIG, TAB, TXT
Series
Accession:
GSE120945
ID:
200120945
5.

IFN-γ selectively suppresses a subset of TLR4-activated genes and enhancers to potentiate M1-like macrophage polarization [RNA-seq]

(Submitter supplied) Complete polarization of macrophages towards an M1-like proinflammatory and antimicrobial state requires combined action of IFN-γ and LPS. Synergistic activation of canonical inflammatory NF-κB target genes by IFN-γ and LPS is well appreciated, but less is known about whether IFN-γ negatively regulates components of the LPS response, and how this affects polarization. A combined transcriptomic and epigenomic approach revealed that IFN-γ selectively abrogates LPS-induced feedback and select metabolic pathways by suppressing TLR4-mediated activation of gene enhancers. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL11154
4 Samples
Download data: TXT
6.

IFN-γ selectively suppresses a subset of TLR4-activated genes and enhancers to potentiate M1-like macrophage polarization [ATAC-seq]

(Submitter supplied) Complete polarization of macrophages towards an M1-like proinflammatory and antimicrobial state requires combined action of IFN-γ and LPS. Synergistic activation of canonical inflammatory NF-κB target genes by IFN-γ and LPS is well appreciated, but less is known about whether IFN-γ negatively regulates components of the LPS response, and how this affects polarization. A combined transcriptomic and epigenomic approach revealed that IFN-γ selectively abrogates LPS-induced feedback and select metabolic pathways by suppressing TLR4-mediated activation of gene enhancers. more...
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL11154
4 Samples
Download data: BIGWIG
Series
Accession:
GSE120942
ID:
200120942
7.

Genome-wide collaboration of canonical and non-canonical STAT1 complexes with NF-κB to control signal integration between Interferons and TLR4 in vascular and immune cells

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Mus musculus
Type:
Genome binding/occupancy profiling by high throughput sequencing; Expression profiling by high throughput sequencing
Platform:
GPL17021
111 Samples
Download data: TDF
Series
Accession:
GSE120808
ID:
200120808
8.

Genome-wide collaboration of canonical and non-canonical STAT1 complexes with NF-κB to control signal integration between Interferons and TLR4 in vascular and immune cells [RNA-seq]

(Submitter supplied) Atherosclerosis is a disease of large and medium-sized muscular arteries and is characterized by vascular inflammation and lipid-laden plaque formation within the intima of the vessel wall. Atherosclerosis is initiated by recruitment of blood leukocytes to the injured vascular endothelium and leads to altered contractility of Vascular Smooth Muscle Cells (VSMCs), acute and chronic luminal obstruction, abnormalities of blood flow and diminished oxygen supply to target organs. more...
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL17021
81 Samples
Download data
Series
Accession:
GSE120807
ID:
200120807
9.

Genome-wide collaboration of canonical and non-canonical STAT1 complexes with NF-κB to control signal integration between Interferons and TLR4 in vascular and immune cells [ChIP-seq]

(Submitter supplied) Atherosclerosis is a disease of large and medium-sized muscular arteries and is characterized by vascular inflammation and lipid-laden plaque formation within the intima of the vessel wall. Atherosclerosis is initiated by recruitment of blood leukocytes to the injured vascular endothelium and leads to altered contractility of Vascular Smooth Muscle Cells (VSMCs), acute and chronic luminal obstruction, abnormalities of blood flow and diminished oxygen supply to target organs. more...
Organism:
Mus musculus
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL17021
30 Samples
Download data: TDF
Series
Accession:
GSE120806
ID:
200120806
10.

Transcript dynamics in classically and alternatively activated macrophages

(Submitter supplied) Using RNA-seq, we have reported that signaling crosstalk among IFN-γ and LPS is integrated at the level of transcriptome and have associated with TFs and TcoFs changes. In addition, we also argue that the transcriptional differences between BMDMs and RAW264.7 macrophage cell line as well as IL-4 and IL-13 on M2 macrophages activation.
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL17021
25 Samples
Download data: TAB
Series
Accession:
GSE103958
ID:
200103958
11.

Genome-wide analysis of bone marrow-derived macrophage (BMDM) priming by Ifng and Ifnb.

(Submitter supplied) Macrophages are a heterogeneous population of immune cells, which are critical for both the initiation and resolution of inflammation. Pro-inflammatory macrophages can be induced by the Th1 cytokine IFNγ and/or TLR triggers, like LPS. Here, we investigated the effects of IFNγ priming on LPS-induced gene expression in primary mouse macrophages.
Organism:
Mus musculus
Type:
Expression profiling by array
Dataset:
GDS5623
Platform:
GPL6885
15 Samples
Download data: TXT
Series
Accession:
GSE60290
ID:
200060290
12.
Full record GDS5623

Interferon-gamma effect on lipopolysaccharide-activated bone marrow-derived macrophages

Analysis of BMDMs primed with IFNγ and subsequently activated with LPS. Pro-inflammatory macrophages are induced by the Th1 cytokine IFNγ and/or the toll-like receptor ligand LPS. Results provide insight into the molecular effects of IFNγ priming on LPS-induced inflammation in macrophages.
Organism:
Mus musculus
Type:
Expression profiling by array, transformed count, 2 agent, 3 protocol sets
Platform:
GPL6885
Series:
GSE60290
15 Samples
Download data
DataSet
Accession:
GDS5623
ID:
5623
13.

Role of CDK8 in interferon-gamma-induced gene expression

(Submitter supplied) Gene regulation by cytokine-activated STAT transcription factors requires serine phosphorylation within the transactivation domain (TAD). STAT1 and STAT3 TAD phosphorylation was reported to occur upon promoter binding by an unknown kinase. Here we show that the Mediator CDK8 module phosphorylates S727 of the STAT1 TAD in the interferon (IFN) signaling pathway as well as the TADs of other STATs. Microarray analysis reveals that CDK8-mediated STAT1 TAD phosphorylation positively or negatively regulates over 40% of IFN-gamma-responsive genes, and RNA polymerase II occupancy correlates with gene expression changes. more...
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL10787
23 Samples
Download data: TXT
Series
Accession:
GSE40728
ID:
200040728
14.

Interferon-γ Represses M2 Gene Expression in Human Macrophages by Disassembling Enhancers Bound by the Transcription Factor MAF

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing; Expression profiling by high throughput sequencing
Platform:
GPL11154
37 Samples
Download data: BED
Series
Accession:
GSE98369
ID:
200098369
15.

IFN-γ Represses M2 Gene Expression in Human Macrophages by Suppressing and Disassembling MAF-binding Enhancers [RNA-seq]

(Submitter supplied) Mechanisms by which IFN-γ activates genes to promote macrophage activation are well studied, but little is known about mechanisms and functions of IFN-γ-mediated gene repression. We used an integrated transcriptomic and epigenomic approach to analyze chromatin accessibility, histone modifications, transcription factor binding, and gene expression in IFN-γ-primed human macrophages. IFN-γ suppressed basal expression of genes corresponding to an ‘M2’-like homeostatic/reparative phenotype. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL11154
16 Samples
Download data: TXT
16.

IFN-γ Represses M2 Gene Expression in Human Macrophages by Suppressing and Disassembling MAF-binding Enhancers [ChIP-seq]

(Submitter supplied) Mechanisms by which IFN-γ activates genes to promote macrophage activation are well studied, but little is known about mechanisms and functions of IFN-γ-mediated gene repression. We used an integrated transcriptomic and epigenomic approach to analyze chromatin accessibility, histone modifications, transcription factor binding, and gene expression in IFN-γ-primed human macrophages. IFN-γ suppressed basal expression of genes corresponding to an ‘M2’-like homeostatic/reparative phenotype. more...
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL11154
17 Samples
Download data: BED
Series
Accession:
GSE98367
ID:
200098367
17.

IFN-γ Represses M2 Gene Expression in Human Macrophages by Suppressing and Disassembling MAF-binding Enhancers [ATAC-seq]

(Submitter supplied) Mechanisms by which IFN-γ activates genes to promote macrophage activation are well studied, but little is known about mechanisms and functions of IFN-γ-mediated gene repression. We used an integrated transcriptomic and epigenomic approach to analyze chromatin accessibility, histone modifications, transcription factor binding, and gene expression in IFN-γ-primed human macrophages. IFN-γ suppressed basal expression of genes corresponding to an ‘M2’-like homeostatic/reparative phenotype. more...
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL11154
4 Samples
Download data: BED
Series
Accession:
GSE98365
ID:
200098365
18.

Expression data from rheumatoid arthritis synovial macrophages

(Submitter supplied) Macrophages from RA synovial fluids were compared to primary human monocyte-derived macrophages.
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL570
14 Samples
Download data: CEL
Series
Accession:
GSE97779
ID:
200097779
19.

Genome wide expression analysis of bone marrow derived macrophage cells (BMDMs) stimulated with IFNg and effect of Batf2 knockdown in BMDMs stimulated with IFNg

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL6887
36 Samples
Download data
Series
Accession:
GSE59210
ID:
200059210
20.

Genome wide expession analysis of effect of Batf2 knock down in bone marrow derived macrophage cells stimulated with IFNg

(Submitter supplied) Bmdm cells were differentiated for 10 days and harvested and culture in six well plate followed by transfection with Batf2 ShRNA. Media was replanished in every two days and on 10th day cells were stimulated with IFNg for 4 hrs. Total RNA was obtain after 4 hrs of stimulation.
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL6887
12 Samples
Download data: TXT
Series
Accession:
GSE59209
ID:
200059209
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