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Links from GEO DataSets

Items: 17

1.
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
2.

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
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.

Synergistic Activation of Inflammatory Cytokine Genes by Priming of Regulatory DNA Elements for Increased Transcription in Response to TLR Signaling

(Submitter supplied) Synergistic activation of inflammatory cytokine genes by IFN-gamma and TLR signaling is important for innate immunity and inflammatory disease pathogenesis, but underlying mechanisms are not known. By obtaining over three billion bases of sequence from chromatin immunoprecipitated DNA, we generated genome-wide chromatin-state maps of human primary monocytes under IFN-gamma-priming and TLR stimulation. more...
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL11154
21 Samples
Download data: TXT, WIG
Series
Accession:
GSE43036
ID:
200043036
13.

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
14.
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
15.

ATF7 mediates lipopolysaccharide-induced epigenetic changes in macrophages involved in innate immunological memory

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Mus musculus
Type:
Expression profiling by array; Genome binding/occupancy profiling by genome tiling array
9 related Platforms
37 Samples
Download data: CEL
Series
Accession:
GSE71113
ID:
200071113
16.

ATF7 mediates lipopolysaccharide-induced epigenetic changes in macrophages involved in innate immunological memory (ChIP)

(Submitter supplied) Immunological memory is generally thought to be mediated exclusively by lymphocytes such as memory T and B cells. However, enhanced innate immune responses caused by a previous infection increase protection against reinfection suggesting the presence of innate immunological memory. Here, we describe 3,811 ATF7 binding sites in mouse peritoneal macrophages, and 95% of the ATF7 signals in wild-type macrophages are lost in ATF7 knockout macrophages. more...
Organism:
Mus musculus
Type:
Genome binding/occupancy profiling by genome tiling array
8 related Platforms
9 Samples
Download data: BED, CEL
Series
Accession:
GSE71112
ID:
200071112
17.

ATF7 mediates lipopolysaccharide-induced epigenetic changes in macrophages involved in innate immunological memory (expression)

(Submitter supplied) Immunological memory is generally thought to be mediated exclusively by lymphocytes such as memory T and B cells. However, enhanced innate immune responses caused by a previous infection increase protection against reinfection suggesting the presence of innate immunological memory. Here, we describe expression profile of peritoneal macrophages from wild-type mice pre-administrated with TLR ligands or from ATF7 knockout mice. more...
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL6246
28 Samples
Download data: CEL
Series
Accession:
GSE71111
ID:
200071111
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