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Links from GEO DataSets

Items: 20

1.
Full record GDS1365

IFN-gamma primed macrophage response to IFN-gamma restimulation: time course

Analysis of CD14+ monocytes primed with 3 U/ml (subactivating dose) IFN-gamma for 48 hours and restimulated with 100 U/ml (saturating dose) IFN-gamma for various time point up to 24 hours. Results provide insight into the influence of IFN-gamma priming on IFN-gamma induced transcriptional responses.
Organism:
Homo sapiens
Type:
Expression profiling by array, count, 2 other, 2 protocol, 3 time sets
Platform:
GPL8300
Series:
GSE1925
18 Samples
Download data
DataSet
Accession:
GDS1365
ID:
1365
2.

IFN-gamma priming

(Submitter supplied) IFN-gamma transcriptional responses in control and IFN-gamma primed primary human macrophages Keywords: repeat sample
Organism:
Homo sapiens
Type:
Expression profiling by array
Dataset:
GDS1365
Platform:
GPL8300
18 Samples
Download data
Series
Accession:
GSE1925
ID:
200001925
3.

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
4.

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
5.

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
6.

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
7.

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
8.

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
9.

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
10.

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
11.

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
12.

Expression data from RAW 264.7 macrophage

(Submitter supplied) IFNg is a pro-inflammatory and pro-atherogenic cytokine that leads to macrophage activation. Adenosine has well-documented anti-inflammatory properties. We used microarrays to compare the global gene expression profile in mouse macrophages stimulated with IFNg alone and those cells treated with IFNg and adenosine. We determined that adenosine suppressed the expression of many IFNg-regulated pro-inflammatory cytokines, chemokines, and other pro-atherogenic genes. more...
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL339
2 Samples
Download data: CEL
Series
Accession:
GSE14612
ID:
200014612
13.

Tassiulas IFN Array v1.0

(Submitter supplied) Type I IFN-inducible gene expression in human blood monocytes primed with Type II IFN. Keywords: repeat sample
Organism:
Homo sapiens
Type:
Expression profiling by array
Dataset:
GDS776
Platform:
GPL8300
12 Samples
Download data
Series
Accession:
GSE1740
ID:
200001740
14.
Full record GDS776

Interferon-alpha effect on monocytes primed with interferon-gamma

Expression profiling of monocytes cultured for 2 days with 150 pg/ml interferon (IFN) gamma and then stimulated with 25 ng/ml of IFN-alpha. Monocytes obtained from 3 donors. Results provide insight into mechanisms underlying the enhanced response of IFN primed monocytes to cytokines.
Organism:
Homo sapiens
Type:
Expression profiling by array, count, 2 agent, 2 protocol sets
Platform:
GPL8300
Series:
GSE1740
12 Samples
Download data
DataSet
Accession:
GDS776
ID:
776
15.

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
16.

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
17.
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
18.

Dissecting primary (translation independent) from secondary (translation dependent) IFN-mediated differential gene expression

(Submitter supplied) NIH-3T3 cells were pretreated for 15 min with either DMSO (mock) or cycloheximide followed by addition of either mock, 100 U/ml IFNalpha or 100 U/ml IFNgamma for 1h. During the last 30 min, 500 µM 4-thiouridine was added to cell culture medium. Total cellular RNA was isolated using Trizol reagent and nascent RNA was purified as described (Dölken et al. RNA 2008) . Three replicates of nascent RNA were analyzed by Affymetrix Mouse Gene ST 1.0 arrays
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL1261
18 Samples
Download data: CEL
Series
Accession:
GSE30457
ID:
200030457
19.

The Myc-Associated Zinc Finger Protein (MAZ) controls STAT1-mediated antiviral response by reshaping epigenome

(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; Methylation profiling by high throughput sequencing
Platform:
GPL11154
66 Samples
Download data: BW, TXT
Series
Accession:
GSE215083
ID:
200215083
20.

The Myc-Associated Zinc Finger Protein (MAZ) controls STAT1-mediated antiviral response by reshaping epigenome [MeDIP-Seq]

(Submitter supplied) The objectives of this study are to understand the regulatory roles of MAZ in biological processes using the NGS-deriveed ChIP-seq, DNA-MEDIP-seq and RNA-seq data in HAP1 control cells and MAZ knockout cells. Our comparative analysis of these data generated from the HAP1 control and MAZ KO cells shows that MAZ is required for recruiting STAT1 to its target sites by reshaping epigenetic landscape in the human genome, thereby mediating antiviral response cells. more...
Organism:
Homo sapiens
Type:
Methylation profiling by high throughput sequencing
Platform:
GPL11154
4 Samples
Download data: BW
Series
Accession:
GSE215082
ID:
200215082
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