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Links from GEO DataSets

Items: 12

1.

Genome-wide gene expression analysis of the whole blood leukocyte transcriptional response to endotoxin treatment

(Submitter supplied) Several inflammatory diseases respond to TNFα inhibitors, implicating TNFα signaling in the pathogenesis of these conditions. Here, we set out to map the systemic genome-wide transcriptome influenced by TNFα release. We performed an intravenous endotoxin challenge in 16 healthy subjects, half of whom were pretreated with the soluble TNF receptor fusion protein, etanercept. Whole-blood leukocyte total RNA was isolated using the PAXgeneTM tube and PAXgeneTM RNA isolation system (PreAnalytiXTM, Qiagen) as described by the manufacturer. more...
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL6947
30 Samples
Download data: TXT
Series
Accession:
GSE36177
ID:
200036177

PubMed Full text in PMC Similar studies Analyze with GEO2R

2.

Transcriptome kinetics of circulating neutrophils during human experimental endotoxemia

(Submitter supplied) Polymorphonuclear cells (neutrophils) play an important role in the systemic inflammatory response syndrome and the development of sepsis. These cells are essential for the defense against microorganisms, but may also cause tissue damage. Therefore, neutrophil numbers and activity are considered to be tightly regulated. Previous studies have investigated gene transcription during experimental endotoxemia in whole blood and peripheral blood mononuclear cells. more...
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL5175
16 Samples
Download data: CEL
Series
Accession:
GSE35590
ID:
200035590

PubMed Full text in PMC Similar studies Analyze with GEO2R

3.

Data expression in alveolar macrophages induced by lipopolysaccharide in humans

(Submitter supplied) Rationale: Lipopolysaccharide (LPS) is ubiquitous in the environment. Inhalation of LPS has been implicated in the pathogenesis and/or severity of several lung diseases, including pneumonia, chronic obstructive pulmonary disease and asthma. Alveolar macrophages are the main resident leukocytes exposed to inhaled antigens. Objectives: To obtain insight into which innate immune pathways become activated within human alveolar macrophages upon exposure to LPS in vivo.
Organism:
Homo sapiens
Type:
Expression profiling by array
Dataset:
GDS4419
Platform:
GPL570
14 Samples
Download data: CEL
Series
Accession:
GSE40885
ID:
200040885

PubMed Full text in PMC Similar studies Analyze with GEO2R

4.
Full record GDS4419

Alveolar macrophage response to bacterial endotoxin lipopolysaccharide exposure in vivo

Analysis of alveolar macrophages purified from bilateral bronchoalveolar lavage after saline instillation into a lung segment followed by LPS instillation into the contralateral lung. Results provide insight into innate immune pathways activated in alveolar macrophages exposed to LPS in vivo.
Organism:
Homo sapiens
Type:
Expression profiling by array, count, 7 individual, 2 stress sets
Platform:
GPL570
Series:
GSE40885
14 Samples
Download data: CEL
DataSet
Accession:
GDS4419
ID:
4419

PubMed Full text in PMC Similar studies GEO Profiles Analyze DataSet

5.

A549 parenchymal cell activation

(Submitter supplied) Alveolar epithalial cells (A549) were used as a model of pulmonary parenchymal cell activation to quiery gene expression profile of activation with either cyclic stretch (20% elongation), TNF (20 ng/ml), LPS (1 mcg/ml) or TNF+STRETCH at both 1 and 4 hrs. Keywords: time-course
Organism:
Homo sapiens
Type:
Expression profiling by array
Dataset:
GDS852
Platform:
GPL201
20 Samples
Download data: CEL, EXP
Series
Accession:
GSE1541
ID:
200001541

PubMed Similar studies Analyze with GEO2R

6.
Full record GDS852

Alveolar epithelial cell line A549 response to acute lung injury causing stimuli: time course

Examination of alveolar epithelial A549 cells in models of pulmonary parenchymal cell activation: exposure to tumor necrosis factor-alpha (TNF-alpha), lipopolysaccharide (LPS), or cyclic stretch. Cells examined 1 and 4 hours after exposure to each acute lung injury-causing stimulus.
Organism:
Homo sapiens
Type:
Expression profiling by array, count, 5 protocol, 2 time sets
Platform:
GPL201
Series:
GSE1541
20 Samples
Download data: CEL, EXP
DataSet
Accession:
GDS852
ID:
852

PubMed Similar studies GEO Profiles Analyze DataSet

7.

Drug-induced liver injury

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Homo sapiens; Mus musculus
Type:
Expression profiling by array
Platforms:
GPL13158 GPL14996
116 Samples
Download data: CEL
Series
Accession:
GSE54257
ID:
200054257

PubMed Similar studies Analyze with GEO2R

8.

Expression data from primary mouse hepatocytes treated with Diclofenac

(Submitter supplied) Drug-induced liver injury (DILI) is an important clinical problem. Here we used a genomics approach to establish the critical drug-induced toxicity pathways that act in synergy with the pro-inflammatory cytokine tumor necrosis factor  (TNF) to cause cell death of liver HepG2 cells. Transcriptomics of the cell injury stress response pathways initiated by two hepatoxicants, diclofenac and carbamazepine, revealed the endoplasmic reticulum (ER) stress/translational initiation signaling and Nrf2 antioxidant signaling as two major affected pathways, which was similar to that observed for the majority of ~80 DILI compounds in primary human hepatocytes. more...
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL14996
10 Samples
Download data: CEL
Series
Accession:
GSE54256
ID:
200054256

PubMed Similar studies Analyze with GEO2R

9.

Gene expression data from precision cut human liver slices treated to diclofenac

(Submitter supplied) Drug-induced liver injury (DILI) is an important clinical problem. Here we used a genomics approach to establish the critical drug-induced toxicity pathways that act in synergy with the pro-inflammatory cytokine tumor necrosis factor (TNF) to cause cell death of liver HepG2 cells. Transcriptomics of the cell injury stress response pathways initiated by two hepatoxicants, diclofenac and carbamazepine, revealed the endoplasmic reticulum (ER) stress/translational initiation signaling and Nrf2 antioxidant signaling as two major affected pathways, which was similar to that observed for the majority of ~80 DILI compounds in primary human hepatocytes. more...
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL13158
10 Samples
Download data: CEL
Series
Accession:
GSE54255
ID:
200054255

PubMed Similar studies Analyze with GEO2R

10.

Expression data from human hepatocellular carcinoma cell line HepG2

(Submitter supplied) Drug-induced liver injury (DILI) is an important clinical problem. Here we used a genomics approach to establish the critical drug-induced toxicity pathways that act in synergy with the pro-inflammatory cytokine tumor necrosis factor (TNF) to cause cell death of liver HepG2 cells. Transcriptomics of the cell injury stress response pathways initiated by two hepatoxicants, diclofenac and carbamazepine, revealed the endoplasmic reticulum (ER) stress/translational initiation signaling and Nrf2 antioxidant signaling as two major affected pathways, which was similar to that observed for the majority of ~80 DILI compounds in primary human hepatocytes. more...
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL13158
96 Samples
Download data: CEL
Series
Accession:
GSE54254
ID:
200054254

PubMed Similar studies Analyze with GEO2R

11.

Transcriptome profiling of control and TNFalpha treated HepG2 cells

(Submitter supplied) The proinflammatory cytokine, TNFalpha is critical in maintaining liver homeostasis since it is a major determiner of hepatocyte life and death. Considering this, gene transcription profiling was examined in control and TNFalpha treated HepG2 cells. Results indicated that TNFalpha could significantly alter the expression of a significant number of genes; most of them were functionally distributed among molecular functions like catalytic activity, binding, molecular transducer activity, transporter activity, translation and transcription regulator activities or enzyme regulator activity. more...
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL570
6 Samples
Download data: CEL, CHP
Series
Accession:
GSE12161
ID:
200012161

PubMed Full text in PMC Similar studies Analyze with GEO2R

12.

Genome map of SND1 binding sites by ChIP-chip analysis in human HepG2 cells under inflammatory conditions.

(Submitter supplied) Profiling of promoter occupancy by SND1 coactivator in human hepatoma cells. Control and TNFα-treated HepG2 cells are immunoprecipitated with anti-SND1 antibody and input and immunoprecipitated material were hybridized in an Agilent human promoter microarray
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by genome tiling array
Platform:
GPL14622
6 Samples
Download data: TXT, XLS
Series
Accession:
GSE61539
ID:
200061539

PubMed Full text in PMC Similar studies

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