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accession-icon GSE40498
Temporal induction of immunoregulatory processes coincides with age-dependent resistance to viral-induced type 1 diabetes
  • organism-icon Homo sapiens, Rattus norvegicus
  • sample-icon 39 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Temporal induction of immunoregulatory processes coincides with age-dependent resistance to viral-induced type 1 diabetes.

Alternate Accession IDs

E-GEOD-40498

Sample Metadata Fields

Sex

View Samples
accession-icon GSE40497
Temporal induction of immunoregulatory processes coincides with age-dependent resistance to viral-induced type 1 diabetes [Rat]
  • organism-icon Rattus norvegicus
  • sample-icon 33 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

A need exists for biomarkers in T1D that can 1) sensitively and specifically detect disease-related immune activity prior to, and independent of, measurement of auto-antibodies towards islet cell antigens; 2) define immunopathological mechanisms; and 3) monitor changes in the inflammatory state associated with disease progression or response to therapeutic intervention. In an effort to fill this gap, we have applied a novel bioassay to both human and BB rat T1D whereby the complex milieu of inflammatory mediators present in plasma can be indirectly detected through their ability to drive transcription in peripheral blood mononuclear cells (PBMCs) drawn from healthy, unrelated donors. The resultant gene expressions are comprehensively measured with a microarray. In our human studies, we find that plasma of recent-onset T1D patients induces expression of a pro-inflammatory signature consisting in part of many interleukin-1 (IL-1) regulated genes related to immunological activation and immunocyte chemotaxis compared to unrelated healthy controls. This signature has been found to resolve in long-standing T1D subjects (>10 years post-onset), thus associating it with active autoimmunity. Importantly, this signature has been detected in pre-onset samples of progressors to T1D years prior to onset and prior to development of auto-antibodies directed towards islet antigens.

Publication Title

Temporal induction of immunoregulatory processes coincides with age-dependent resistance to viral-induced type 1 diabetes.

Alternate Accession IDs

E-GEOD-40497

Sample Metadata Fields

Sex

View Samples
accession-icon GSE40496
Temporal induction of immunoregulatory processes coincides with age-dependent resistance to viral-induced type 1 diabetes [human]
  • organism-icon Homo sapiens
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

A need exists for biomarkers in T1D that can 1) sensitively and specifically detect disease-related immune activity prior to, and independent of, measurement of auto-antibodies towards islet cell antigens; 2) define immunopathological mechanisms; and 3) monitor changes in the inflammatory state associated with disease progression or response to therapeutic intervention. In an effort to fill this gap, we have applied a novel bioassay to both human and BB rat T1D whereby the complex milieu of inflammatory mediators present in plasma can be indirectly detected through their ability to drive transcription in peripheral blood mononuclear cells drawn from healthy, unrelated donors. The resultant gene expressions are comprehensively measured with a microarray. In our human studies, we find that plasma of recent-onset T1D patients induces expression of a pro-inflammatory signature consisting in part of many interleukin-1 (IL-1) regulated genes related to immunological activation and immunocyte chemotaxis compared to unrelated healthy controls. This signature has been found to resolve in long-standing T1D subjects (>10 years post-onset), thus associating it with active autoimmunity. Importantly, this signature has been detected in pre-onset samples of progressors to T1D years prior to onset and prior to development of auto-antibodies directed towards islet antigens.

Publication Title

Temporal induction of immunoregulatory processes coincides with age-dependent resistance to viral-induced type 1 diabetes.

Alternate Accession IDs

E-GEOD-40496

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon GSE19537
Identification of a Serum Induced Transcriptional Signature Associated with Type 1 Diabetes in the BioBreeding Rat
  • organism-icon Rattus norvegicus
  • sample-icon 53 Downloadable Samples
  • Technology Badge Icon Affymetrix Rat Genome 230 2.0 Array (rat2302)

Description

Human type 1 diabetes (T1D) arises through autoimmunity towards the insulin-producing pancreatic cells and is modeled by the BioBreeding (BB) rat. Factors associated with islet autoimmunity are dilute and difficult to directly measure in the periphery. Therefore, we previously utilized microarray-based bioassay where human T1D sera were used to induce a disease-specific gene expression signature in unrelated, healthy peripheral blood mononuclear cells (PBMC).

Publication Title

Identification of a serum-induced transcriptional signature associated with type 1 diabetes in the BioBreeding rat.

Alternate Accession IDs

E-GEOD-19537

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon GSE24695
Transcription Factor Redundancy Ensures Induction of the Antiviral State
  • organism-icon Mus musculus, Homo sapiens
  • sample-icon 13 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A 2.0 Array (hgu133a2)

Description

Transcriptional response to virus infection in mice lacking type I and type III signaling

Publication Title

Transcription factor redundancy ensures induction of the antiviral state.

Alternate Accession IDs

E-GEOD-24695

Sample Metadata Fields

Specimen part, Cell line, Treatment

View Samples
accession-icon GSE64337
Inhibition of de novo Palmitate Synthesis by Fatty Acid Synthase Induces Apoptosis in Tumor Cells by Remodeling Cell Membranes, Inhibiting Signaling Pathways, and Reprogramming Gene Expression
  • organism-icon Homo sapiens
  • sample-icon 9 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

TVB-3166, an orally available, reversible, potent, and selective FASN inhibitors, was used to investigate FASN as a cancer therapeutic target. FASN inhibition with TVB-3166 induces apoptosis, inhibits anchorage-independent cell growth under lipid-rich conditions, and inhibits in vivo xenograft tumor growth.

Publication Title

Inhibition of de novo Palmitate Synthesis by Fatty Acid Synthase Induces Apoptosis in Tumor Cells by Remodeling Cell Membranes, Inhibiting Signaling Pathways, and Reprogramming Gene Expression.

Alternate Accession IDs

E-GEOD-64337

Sample Metadata Fields

Treatment

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accession-icon GSE15139
Identification of genes effected by GM-CSF treatment in mature human neutrophils
  • organism-icon Homo sapiens
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U95 Version 2 Array (hgu95av2)

Description

The objective of this study was to compare the transcriptional repertoire of mature human neutrophils before and after GM-CSF treatment by using oligonucleotide microarrays.

Publication Title

RhoH/TTF negatively regulates leukotriene production in neutrophils.

Alternate Accession IDs

E-GEOD-15139

Sample Metadata Fields

Specimen part

View Samples
accession-icon GSE54387
Expression data from induced pluripotent stem cell-derived endothelial cells from healthy and diet-induced obesity mice
  • organism-icon Mus musculus
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Little is known about the function of induced pluripotent stem cell-derived endothelial cells (iPSC-ECs) generated from diabetics, as this could potentially limit subsequent therapeutic use in this patient population.

Publication Title

Pravastatin reverses obesity-induced dysfunction of induced pluripotent stem cell-derived endothelial cells via a nitric oxide-dependent mechanism.

Alternate Accession IDs

E-GEOD-54387

Sample Metadata Fields

Age, Specimen part

View Samples
accession-icon SRP068418
Targeted deletion of circadian clock gene Arntl in the nephron results in dysregulation of diverse metabolic pathways
  • organism-icon Mus musculus
  • sample-icon 12 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500, Illumina HiSeq 2000

Description

The circadian clock controls a wide variety of metabolic and homeostatic processes in a number of tissues, including the kidney. However, the role of the renal circadian clocks remains largely unknown. To address this question we performed transcriptomic analysis in mice with inducible and conditional ablation of the circadian clock system in the renal tubular cells (Bmal1lox/lox/Pax8-rtTA/LC1 mice). Deep sequencing of the renal transcriptome revealed significant changes in the expression of genes related to metabolic pathways and organic anion transport. In parallel, kidneys from Bmal1lox/lox/Pax8-rtTA/LC1 mice exhibited a significant decrease in the NAD+/NADH ratio suggesting an increased anaerobic glycolysis and/or decreased mitochondrial function. In-depth analysis of two selected pathways revealed (i) a significant increase in plasma urea levels correlating with increased renal arginase 2 (Arg2) activity, hyperargininemia and increase of the kidney arginine content; (ii) a significantly increased plasma creatinine concentration and reduced capacity of the kidney to secrete anionic drugs (furosemide), paralleled by a ~80% decrease in the expression levels of organic anion transporter OAT3 (SLC22a8). Collectively, these results indicate that the renal circadian clocks control a variety of metabolic/homeostatic processes at both the intra-renal and systemic levels and are involved in drug disposition. Overall design: Mice with a specific ablation of the Arntl gene encoding BMAL1 in the renal tubular cells were compared to wild-type littermate at ZT4 and ZT16 (ZT – Zeitgeber time units; ZT0 is the time of light on and ZT12 is the time of light off).

Publication Title

Nephron-Specific Deletion of Circadian Clock Gene Bmal1 Alters the Plasma and Renal Metabolome and Impairs Drug Disposition.

Alternate Accession IDs

GSE76838

Sample Metadata Fields

Specimen part, Subject, Time

View Samples
accession-icon SRP107968
Integrative epigenomic analyses of early-life hypothalamic response to augmented maternal care [RNA-seq]
  • organism-icon Rattus norvegicus
  • sample-icon 6 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

The quality of maternal care in early-life plays a crucial role in mammalian neurodevelopment. Augmented maternal care (AMC) is a well-established rodent model of enhanced neonatal care. Rats that have undergone AMC have improved stress resilience and cognition compared with rats that have experienced normal levels of maternal care or adverse neonatal stress. However, the epigenomic basis of long-lived responses to AMC has not been previously explored. Thus, we employed whole-genome bisulfite sequencing (WGBS), RNA-sequencing (RNA-seq), and a multiplex microRNA (miRNA) assay to assess DNA cytosine methylation, gene expression, and miRNA expression, respectively. The integrated results identify a suite of 20 prioritized candidates impacted by AMC. Overall, these results identified AMC-induced regulatory differences in genes related to neurotransmission, neurodevelopment, protein synthesis, and oxidative phosphorylation in addition to the expected stress response genes. Together, these unbiased results represent a key progression in understanding the complex mechanisms underlying the early-life mechanisms for AMC programming stress resiliency. Overall design: DNA methylation and RNA were assayed in augmented maternal care male rats as well as controls.

Publication Title

Experience-dependent neuroplasticity of the developing hypothalamus: integrative epigenomic approaches.

Alternate Accession IDs

GSE99278

Sample Metadata Fields

Sex, Specimen part, Treatment, Subject

View Samples
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refine.bio is a repository of uniformly processed and normalized, ready-to-use transcriptome data from publicly available sources. refine.bio is a project of the Childhood Cancer Data Lab (CCDL)

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Cite refine.bio

Casey S. Greene, Dongbo Hu, Richard W. W. Jones, Stephanie Liu, David S. Mejia, Rob Patro, Stephen R. Piccolo, Ariel Rodriguez Romero, Hirak Sarkar, Candace L. Savonen, Jaclyn N. Taroni, William E. Vauclain, Deepashree Venkatesh Prasad, Kurt G. Wheeler. refine.bio: a resource of uniformly processed publicly available gene expression datasets.
URL: https://www.refine.bio

Note that the contributor list is in alphabetical order as we prepare a manuscript for submission.

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