GEO DataSets

Analysis of pancreas of 3-week-old BDC2.5 transgenics that express a diabetogenic T cell receptor on the NOD or NOD.scid genetic background. BDC2.5/NOD has severe insulitis. BDC2.5/NOD.scid has severe insulitis and type 1 diabetes (T1D). Result provides insight into the pathogenesis of T1D.

Organism:

Mus musculus

Type:

Expression profiling by array, transformed count, 3 disease state, 4 strain sets

Platform:

GPL81

Series:

GSE1623

8 Samples

Download data: CEL

(Submitter supplied) Total pancreatic RNA was isolated from 3 week old NOD.scid, NOD, BDC2.5/NOD and BDC2.5/NOD.scid animals by GITC method. Targets were produced using standard Affymetrix procedures from about 10ug total RNA. The data from NOD.scid, NOD, BDC2.5/NOD and BDC2.5/NOD.scid Affymetrix MGU74Av2 cel files was converted into Robust Multi Array (RMA) text file for analysis using GeneSpring 6.1 Keywords: other

Organism:

Mus musculus

Type:

Expression profiling by array

Dataset:

GDS1533

Platform:

GPL81

8 Samples

Download data: CEL

(Submitter supplied) In this study, we performed the gene expression analysis of the Normal, Diabetic and AAT treated NOD mice to elucidate the transcriptional changes induced by AAT. This will assist in identifying the biological processes / pathways involved in curative mechanism of AAT. Keywords: alpha1 antitrypsin treatment

Organism:

Mus musculus

Type:

Expression profiling by array

Platform:

GPL1261

6 Samples

Download data: CEL

(Submitter supplied) BDC2.5/NOD mice were treated with cyclophosphamide to induce type 1 diabetes. Their pancreatic islets were analyzed before treatment (Day 0) and as treatment progressed (Days 1 through 3) Keywords = type I diabetes Keywords = cyclophosphamide Keywords = BDC2.5 Keywords = NOD Keywords = pancreas Keywords = islets Keywords: time-course

Organism:

Mus musculus

Type:

Expression profiling by array

Dataset:

GDS1056

Platform:

GPL81

18 Samples

Download data

Analysis of pancreatic islets from BDC2.5/NOD transgenics after treatment with 200 mg/kg cyclophosphamide (CY) at various time points up to 3 days. CY induces diabetes in BDC2.5/NOD transgenics. Results provide insight into molecular events accompanying the progression from insulitis to diabetes.

Organism:

Mus musculus

Type:

Expression profiling by array, count, 2 agent, 4 time sets

Platform:

GPL81

Series:

GSE2254

18 Samples

Download data

(Submitter supplied) Type 1 diabetes (T1D) is a chronic autoimmune disease that involves immune mediated destruction of β cells. How β cells respond to immune attack is unknown. We identified a population of β cells during the progression of T1D in non-obese diabetic (NOD) mice that survives immune attack. This population develops from normal β cells confronted with islet infiltrates. Pathways involving cell movement, growth and proliferation, immune responses, and cell death and survival are activated in these cells. more...

Organism:

Mus musculus

Type:

Expression profiling by high throughput sequencing

Platform:

GPL13112

8 Samples

Download data: TXT

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.

Organism:

Homo sapiens

Type:

Methylation profiling by genome tiling array; Expression profiling by high throughput sequencing

Platforms:

GPL13534 GPL11154

12 Samples

Download data: TXT

(Submitter supplied) Type 1 diabetes (T1D) is caused by autoimmune destruction of pancreatic β cells. Mounting evidence supports a central role for β-cell alterations in triggering the activation of self-reactive T-cells in T1D. However, the early deleterious events that occur in β cells, underpinning islet autoimmunity are not known. We hypothesized that epigenetic modifications induced in β cells by inflammatory mediators play a key role in initiating the autoimmune response. more...

Organism:

Homo sapiens

Type:

Expression profiling by high throughput sequencing

Platform:

GPL11154

6 Samples

Download data: TXT

(Submitter supplied) Type 1 diabetes (T1D) is caused by autoimmune destruction of pancreatic β cells. Mounting evidence supports a central role for β-cell alterations in triggering the activation of self-reactive T-cells in T1D. However, the early deleterious events that occur in β cells, underpinning islet autoimmunity are not known. We hypothesized that epigenetic modifications induced in β cells by inflammatory mediators play a key role in initiating the autoimmune response. more...

Organism:

Homo sapiens

Type:

Methylation profiling by genome tiling array

Platform:

GPL13534

6 Samples

Download data: TXT

(Submitter supplied) During Type 1 diabetes development, T lymphocytes infiltrate pancreatic islets and induce the destruction of the insulin-producing cells within the islets, the beta-cells. T lymphocytes are known to secrete pro-inflammatory cytokines but also exosomes that could contribute to the mechanisms leading to beta-cell death. In this project, we wanted to investigate the effect of exosomes released from T lymphocytes on beta-cell gene expression.

Organism:

Mus musculus

Type:

Expression profiling by array

Platform:

GPL11202

6 Samples

Download data: TXT

(Submitter supplied) Background: Epigenetic alteration of the genome has been shown to provide palliative effects in mouse models of certain human autoimmune disorders. We have investigated whether chromatin remodeling could provide protection against autoimmune diabetes in nonobese diabetic (NOD) mice. Treatment of female mice during the transition from prediabetic to diabetic stage (18-24 weeks of age) with the well-characterized histone deacetylase inhibitor, Trichostatin A (TSA) effectively reduced the incidence of diabetes and abrogated the ability of splenocytes to adoptively transfer the disease into immunodeficient NOD.scid mice. more...

Organism:

Mus musculus

Type:

Expression profiling by array

Platform:

GPL1261

6 Samples

Download data: CEL

(Submitter supplied) Prior to the onset of autoimmune destruction, type 1 diabetic patients and an animal model thereof, the nonobese diabetic (NOD) mouse, show morphological and functional abnormalities in target organs, which may act as inciting events for leukocyte infiltration. To better understand these abnormalities, but without the complications associated with inflammatory infiltrates, we examined genes expressed in autoimmune target tissues (pancreas, submandibular glands, and lacrimal glands) of NOD/scid mice and of autoimmune-resistant C57BL6/scid mice. more...

Organism:

Mus musculus

Type:

Expression profiling by array

Datasets:

GDS2177 GDS2178 GDS2179

Platforms:

GPL83 GPL81 GPL82

117 Samples

Download data

Analysis of pancreata and submandibular and lacrimal glands from 6-, 9-, and 15-week-old NOD/scid animals, respectively, before the onset of autoimmune destruction of the tissues. The NOD/scid animal is a model for type 1 diabetes. The three organs examined are autoimmune targets in type 1 diabetes.

Organism:

Mus musculus

Type:

Expression profiling by array, count, 3 age, 2 strain, 3 tissue sets

Platform:

GPL83

Series:

GSE4953

39 Samples

Download data

Analysis of pancreata and submandibular and lacrimal glands from 6-, 9-, and 15-week-old NOD/scid animals, respectively, before the onset of autoimmune destruction of the tissues. The NOD/scid animal is a model for type 1 diabetes. The three organs examined are autoimmune targets in type 1 diabetes.

Organism:

Mus musculus

Type:

Expression profiling by array, count, 3 age, 2 strain, 3 tissue sets

Platform:

GPL82

Series:

GSE4953

39 Samples

Download data

Analysis of pancreata and submandibular and lacrimal glands from 6-, 9-, and 15-week-old NOD/scid animals, respectively, before the onset of autoimmune destruction of the tissues. The NOD/scid animal is a model for type 1 diabetes. The three organs examined are autoimmune targets in type 1 diabetes.

Organism:

Mus musculus

Type:

Expression profiling by array, count, 3 age, 2 strain, 3 tissue sets

Platform:

GPL81

Series:

GSE4953

39 Samples

Download data

(Submitter supplied) Islet leukocytic infiltration (insulitis) is first obvious at around 4 weeks of age in the NOD mouse – a model for human type 1 diabetes (T1DM). The molecular events leading to insulitis are poorly understood. Since TIDM is caused by numerous genes, we hypothesized that multiple molecular pathways are altered and interact to initiate this disease. Analysis of the global gene expression profiles using microarrays followed by hierarchical clustering revealed that the majority (~90%) of the differentially expressed genes in NOD mice relative to control mice were repressed. more...

Organism:

Mus musculus

Type:

Expression profiling by array

Platforms:

GPL340 GPL339

60 Samples

Download data: CEL

(Submitter supplied) Early stages of type 1 diabetes (T1D) are characterized by local autoimmune inflammation and progressive loss of insulin-producing pancreatic β cells. We show here that exposure to pro-inflammatory cytokines unmasks a striking plasticity of the β-cell regulatory landscape. We expand the repertoire of human islet regulatory elements by mapping stimulus-responsive enhancers linked to changes in the β-cell transcriptome, proteome and 3D chromatin structure. more...

Organism:

Homo sapiens

Type:

Other

Platform:

GPL11154

30 Samples

Download data: TXT

(Submitter supplied) Early stages of type 1 diabetes (T1D) are characterized by local autoimmune inflammation and progressive loss of insulin-producing pancreatic β cells. We show here that exposure to pro-inflammatory cytokines unmasks a striking plasticity of the β-cell regulatory landscape. We expand the repertoire of human islet regulatory elements by mapping stimulus-responsive enhancers linked to changes in the β-cell transcriptome, proteome and 3D chromatin structure. more...

Organism:

Homo sapiens

Type:

Genome binding/occupancy profiling by high throughput sequencing

Platform:

GPL11154

16 Samples

Download data: BW

(Submitter supplied) Early stages of type 1 diabetes (T1D) are characterized by local autoimmune inflammation and progressive loss of insulin-producing pancreatic β cells. We show here that exposure to pro-inflammatory cytokines unmasks a striking plasticity of the β-cell regulatory landscape. We expand the repertoire of human islet regulatory elements by mapping stimulus-responsive enhancers linked to changes in the β-cell transcriptome, proteome and 3D chromatin structure. more...

Organism:

Homo sapiens

Type:

Genome binding/occupancy profiling by high throughput sequencing

Platform:

GPL11154

20 Samples

Download data: BW