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accession-icon GSE96062
Expression data from primary adipocytes, ASCs, and ASC-adipocytes with or without IRF1 overexpression
  • organism-icon Homo sapiens
  • sample-icon 16 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Through employing a comparative transcriptomics approach, we identified IRF1 as differentiatlly regulated between primary and in vitro derived genetically matched adipocytes.

Publication Title

Activation of IRF1 in Human Adipocytes Leads to Phenotypes Associated with Metabolic Disease.

Sample Metadata Fields

Specimen part

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accession-icon GSE148702
The effects of SGLT-2 inhibitors canagliflozin on hepatic transcription
  • organism-icon Mus musculus
  • sample-icon 13 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 2.0 ST Array (mogene20st)

Description

We assessed the change in hepatic transciptional pattern after treatment with SGLT-2 inhibitors canagliflozin in a mice model of diet-induced obesity.

Publication Title

SGLT2 inhibition reprograms systemic metabolism via FGF21-dependent and -independent mechanisms.

Sample Metadata Fields

Sex

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accession-icon GSE64770
Expression Profiling In HMDP (high-fat/high-sucrose diet)
  • organism-icon Mus musculus
  • sample-icon 872 Downloadable Samples
  • Technology Badge Icon Affymetrix HT Mouse Genome 430A Array (htmg430a), Illumina MouseRef-8 v2.0 expression beadchip

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Genetic architecture of insulin resistance in the mouse.

Sample Metadata Fields

Sex, Age, Specimen part

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accession-icon GSE64768
Gonadal Adipose Tissue Profiling In HMDP (high-fat/high-sucrose diet)
  • organism-icon Mus musculus
  • sample-icon 439 Downloadable Samples
  • Technology Badge Icon Affymetrix HT Mouse Genome 430A Array (htmg430a), Illumina MouseRef-8 v2.0 expression beadchip

Description

Identify genes in the gonadal adipose tissue whose expression is under genetic regulation in the Hybrid Mouse Diversity Panel (HMDP). The HMDP comprises classical inbred and recombinant inbred wild type mice. The RMA values of genes were used for genome wide association as described in Parks et al Cell Metabolism 2015. These data are used to identify candidate genes at loci associated with obesity and dietary responsiveness.

Publication Title

Genetic architecture of insulin resistance in the mouse.

Sample Metadata Fields

Sex, Age, Specimen part

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accession-icon GSE64769
Liver Profiling In HMDP (high-fat/high-sucrose diet)
  • organism-icon Mus musculus
  • sample-icon 433 Downloadable Samples
  • Technology Badge Icon Affymetrix HT Mouse Genome 430A Array (htmg430a), Illumina MouseRef-8 v2.0 expression beadchip

Description

Identify genes in the liver whose expression is under genetic regulation in the Hybrid Mouse Diversity Panel (HMDP). The HMDP comprises classical inbred and recombinant inbred wild type mice. The RMA values of genes were used for genome wide association as described in Parks et al Cell Metabolism 2015. These data are used to identify candidate genes at loci associated with obesity and dietary responsiveness.

Publication Title

Genetic architecture of insulin resistance in the mouse.

Sample Metadata Fields

Sex, Age, Specimen part

View Samples
accession-icon GSE30041
Programming human pluripotent stem cells into adipocytes
  • organism-icon Homo sapiens
  • sample-icon 34 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

Programming human pluripotent stem cells into white and brown adipocytes.

Sample Metadata Fields

Specimen part, Disease

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accession-icon GSE30038
Programming human pluripotent stem cells into adipocytes [Affymetrix]
  • organism-icon Homo sapiens
  • sample-icon 34 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

The utility of human pluripotent stem cells as a tool for understanding disease and as a renewable source of cells for transplantation therapies is dependent on efficient differentiation protocols that convert these cells into relevant adult cell types. Here we report the robust and efficient differentiation of human pluripotent stem cells into adipocytes. We found that inducible expression of PPARG2 in pluripotent stem cell-derived mesenchymal progenitor cells programmed their development towards an adipocyte cell fate. Using this approach, multiple human pluripotent cell lines were differentiated into adipocytes with efficiencies of 85% to 90%. These pluripotent stem cell-derived adipocytes retained their identity independent of transgene expression, could be maintained in culture for several weeks, expressed mature markers, and exhibited mature functional properties such as lipid catabolism in response to a beta-adrenergic stimulus. Global transcriptional and lipid metabolomic analyses further confirmed the identity and maturity of these pluripotent stem cell-derived adipocytes.

Publication Title

Programming human pluripotent stem cells into white and brown adipocytes.

Sample Metadata Fields

Specimen part

View Samples
accession-icon GSE46600
Transcriptome and Molecular Pathways Analysis of CD4 T-Cells from Young NOD Mice
  • organism-icon Mus musculus
  • sample-icon 44 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Type 1 diabetes is a multigenic disease caused by T-cell mediated destruction of the insulin producing -cells. Although conventional (targeted) approaches of identifying causative genes have advanced our knowledge of this disease, many questions remain unanswered. Using a whole molecular systems study, we unraveled the genes/molecular pathways that are altered in CD4 T-cells from young NOD mice prior to insulitis (lymphocytic infiltration into the pancreas). Many of the CD4 T-cell altered genes lie within known diabetes susceptibility regions (Idd), including several genes in the diabetes resistance region Idd13 and two genes (Khdrbs1 and Ptp4a2) in the CD4 T-cell diabetogenic activity region Idd9/11. Alterations involved apoptosis/cell proliferation and metabolic pathways (predominant at 2 weeks), inflammation and cell signaling/activation (predominant at 3 weeks), and innate and adaptive immune responses (predominant at 4 weeks). We identified several factors that may regulate these abnormalities: IRF-1, HNF4A, TP53, BCL2L1 (lies within Idd13), IFNG, IL4, IL15, and prostaglandin E2, which were common to all 3 ages; AR and IL6 to 2 and 4 weeks; and Interferon (IFN-I) and IRF-7 to 3 and 4 weeks. Others were unique to the various ages (e. g. MYC, JUN, and APP to 2 weeks; TNF, TGFB1, NFKB, ERK, and p38MAPK to 3 weeks; and IL12 and STAT4 to 4 weeks). Our data suggest that diabetes resistance genes in Idd13 and Idd9/11, and BCL2L1, IL6-AR and IFNG-IRF-1-IFN-I/IRF-7-IL12 pathways play an important role in CD4 T-cells in the early pathogenesis of autoimmune diabetes. Thus, the alternative approach of investigation at the molecular systems level has captured new information, which combined with validation studies, offers the opportunity to test hypotheses on the role played by the genes/molecular pathways identified in this study, to understand better the mechanisms of autoimmune diabetes in CD4 T-cells, and to develop new therapeutic strategies for the disease.

Publication Title

Molecular pathway alterations in CD4 T-cells of nonobese diabetic (NOD) mice in the preinsulitis phase of autoimmune diabetes.

Sample Metadata Fields

Age, Specimen part

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accession-icon GSE37450
Molecular Phenotyping of Immune Cells from Young NOD Mice
  • organism-icon Mus musculus
  • sample-icon 60 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Expression 430A Array (moe430a)

Description

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.

Publication Title

Molecular phenotyping of immune cells from young NOD mice reveals abnormal metabolic pathways in the early induction phase of autoimmune diabetes.

Sample Metadata Fields

Age, Specimen part

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accession-icon GSE36507
Gene expression in hypoxia-tolerant Drosophila melanogaster
  • organism-icon Drosophila melanogaster
  • sample-icon 27 Downloadable Samples
  • Technology Badge Icon Affymetrix Drosophila Genome 2.0 Array (drosophila2)

Description

Hypoxia plays a key pathogenic role in the outcome of many pathologic conditions. To elucidate how organisms successfully adapt to hypoxia, a population of Drosophila melanogaster was generated, through an iterative selection process, that is able to complete its lifecycle at 4% O2, a level lethal to the starting parental population. Transcriptomic analysis of flies adapted for >200 generations was performed to identify pathways and processes that contribute to the adapted phenotype, comparing gene expression of three developmental stages with generation-matched control flies. A third group was included, hypoxia-adapted flies reverted to 21% O2 for five generations, to address the relative contributions of genetics and hypoxic environment to the gene expression differences. We identified the largest number of expression differences in 0.5-3 hr post-eclosion adult flies that were hypoxia-adapted and maintained in 4% O2, and found evidence that changes in Wnt signaling contribute to hypoxia tolerance in flies.

Publication Title

Wnt pathway activation increases hypoxia tolerance during development.

Sample Metadata Fields

No sample metadata fields

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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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