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Links from GEO DataSets

Items: 20

1.

Dendritic cell stimulation: 5 ligands, 9 time points

(Submitter supplied) mouse primary BMDCs were stimulated with tlr ligands and gene expression changes were profiled on Affymetrix arrays
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL8759
96 Samples
Download data: CEL
Series
Accession:
GSE17721
ID:
200017721
2.

Gene Expression data from mouse bone marrow derived macrophages treated with different inflammatory stimuli

(Submitter supplied) The activation profiles of macrophages under different immune and inflammatory conditions have generated great interest. LPS, in particular, is a commonly used in vitro model of infection and inflammation studies in macrophages. We have used gene expression microarrays to define the effects of each of three variables; LPS dose, LPS vs. interferons beta and gamma, and genetic background on the transcriptional response of mouse bone marrow-derived macrophages Macrophages derived from the C57BL/6 strain of mouse were challenged with increasing doses of LPS over a 24 hour time-course (0.5ng/ml, 5ng/ml, or 50ng/ml LPS). more...
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL11533
64 Samples
Download data: CEL
Series
Accession:
GSE44292
ID:
200044292
3.

LPS-induced and E. coli-induced gene expression in wildtype and MyD88-/- mouse macrophages

(Submitter supplied) Comparison of gene expression in wildtype and MyD88-/- C57BL/6J mouse macrophages treated with 10 ng/mL LPS for 2 hours versus media treated control macrophages, and, wildtype and MyD88-/- C57BL/6J mouse macrophages treated with live E. coli bacteria (log phase; 1 bact per 1 macrophage) for 2 hours versus media treated control macrophages. Cells from 4 mice of each geneotype were used and each individual provided its own control. more...
Organism:
Mus musculus
Type:
Expression profiling by array
Datasets:
GDS1705 GDS1706
Platform:
GPL1226
31 Samples
Download data
Series
Accession:
GSE1405
ID:
200001405
4.
Full record GDS1706

MyD88-deficient macrophage response to lipopolysaccharide and E. coli (dye swap)

Analysis of MyD88 null mutant macrophages treated with LPS or live E. coli. MyD88 transduces cell signaling events downstream of Toll-like receptors, a key component of host defense. Results suggest most of the host response to endotoxin or live bacteria is actually regulated independently of MyD88.
Organism:
Mus musculus
Type:
Expression profiling by array, log2 ratio, 2 agent, 2 genotype/variation sets
Platform:
GPL1226
Series:
GSE1405
15 Samples
Download data
DataSet
Accession:
GDS1706
ID:
1706
5.
Full record GDS1705

MyD88-deficient macrophage response to lipopolysaccharide and E. coli

Analysis of MyD88 null mutant macrophages treated with LPS or live E. coli. MyD88 transduces cell signaling events downstream of Toll-like receptors, a key component of host defense. Results suggest most of the host response to endotoxin or live bacteria is actually regulated independently of MyD88.
Organism:
Mus musculus
Type:
Expression profiling by array, log2 ratio, 2 agent, 2 genotype/variation sets
Platform:
GPL1226
Series:
GSE1405
16 Samples
Download data
DataSet
Accession:
GDS1705
ID:
1705
6.

Transcription of Tnfaip3 is regulated by NF-kB and p38 via C/EBPβ in activated macrophages

(Submitter supplied) Macrophages play a pivotal role in the immune system through recognition and elimination of microbial pathogens. Toll-like receptors (TLRs) on macrophages interact with microbial substances and initiate signal transduction through intracellular adapters. TLR4, which is important for the response to lipopolysaccharide (LPS), triggers downstream signaling mediators and eventually activates IkB kinase (IKK) complex and mitogen-activated protein kinases (MAPKs) such as p38. more...
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL6885
24 Samples
Download data: TXT
Series
Accession:
GSE46361
ID:
200046361
7.

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
8.

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
9.

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
10.

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
11.

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
12.

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
13.

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
14.

Mouse ischemic tolerance genomic analysis of the brain and blood.

(Submitter supplied) Ischemic tolerance can be induced by numerous preconditioning stimuli, including various Toll-like receptor (TLR) ligands. We have shown previously that systemic administration of the TLR4 ligand, lipopolysaccharide (LPS) or the TLR9 ligand, unmethylated CpG ODNs prior to transient brain ischemia in mice confers substantial protection against ischemic damage. To elucidate the molecular mechanisms of preconditioning, we compared brain and blood genomic profiles in response to preconditioning with these TLR ligands and to preconditioning via exposure to brief ischemia. more...
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL1261
224 Samples
Download data: CEL
Series
Accession:
GSE32529
ID:
200032529
15.

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
16.

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
17.

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
18.

Chronic exposure to fluticasone propionate shapes gene expression and modulates innate and adaptive activation pathways in human macrophages

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL10558
24 Samples
Download data
Series
Accession:
GSE49852
ID:
200049852
19.

Chronic exposure to fluticasone propionate shapes gene expression and modulates innate and adaptive activation pathways in human macrophages (LPS)

(Submitter supplied) Here we investigate how glucocorticoids affect the response to LPS in human macrophages.
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL10558
12 Samples
Download data: TXT
Series
Accession:
GSE49709
ID:
200049709
20.

Chronic exposure to fluticasone propionate shapes gene expression and modulates innate and adaptive activation pathways in human macrophages (INF)

(Submitter supplied) Here we investigate how glucocorticoids affect the response to Interferon gamma in human macrophages.
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL10558
12 Samples
Download data: TXT
Series
Accession:
GSE49706
ID:
200049706
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