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accession-icon GSE47065
Gene expression profiling of IR-/-, IGF-1R-/- (dKO) newborn epidermis.
  • organism-icon Mus musculus
  • sample-icon 8 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Analysis of newborn mouse epidermis lacking the expression of Insulin receptor (IR) and Insulin like growth factor 1 receptor (IGF-1R). Results show that IR/IGF-1R signalling control epidermal morphogenesis.

Publication Title

Insulin/IGF-1 controls epidermal morphogenesis via regulation of FoxO-mediated p63 inhibition.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE21710
Insulin receptor signaling in osteoblasts regulates postnatal bone acquisition and body composition
  • organism-icon Mus musculus
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Global energy balance in mammals is controlled by the actions of circulating hormones that coordinate fuel production and utilization in metabolically active tissues. Bone-derived osteocalcin, in its undercarboxylated, hormonal form, regulates fat deposition and is a potent insulin secretagogue. Here, we show that insulin receptor (IR) signaling in osteoblasts controls osteoblast development and osteocalcin expression by suppressing the Runx2 inhibitor Twist-2. Mice lacking IR in osteoblasts have low circulating undercarboxylated osteocalcin and reduced bone acquisition due to decreased bone formation and deficient numbers of osteoblasts. With age, these mice develop marked peripheral adiposity and hyperglycemia accompanied by severe glucose intolerance and insulin resistance. The metabolic abnormalities in these mice are improved by infusion of exogenous under-carboxylated osteocalcin. These results indicate the existence of a bone-pancreas endocrine loop through which insulin signaling in the osteoblast ensures osteoblast differentiation and stimulates osteocalcin production, which in turn regulates insulin sensitivity and pancreatic insulin secretion to control glucose homeostasis.

Publication Title

Insulin receptor signaling in osteoblasts regulates postnatal bone acquisition and body composition.

Sample Metadata Fields

Specimen part, Time

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accession-icon SRP041341
Gene expression profiles of antigen-specific CD4+ T cells from mice carrying T cell-specific deletions of MyD88 or IL6Ra
  • organism-icon Mus musculus
  • sample-icon 3 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

2W:I-A(b) specific CD4+ T cells were isolated from immunized knock-out mice and wild-type controls on day 7 post immunization and the gene expression profiles of the cells were compared Overall design: Antigen-specifc CD4+ T cells were isolated and pooled from 4 independent experiments. The samples represent antigen-specific T cells from 15-30 mice per genotype.

Publication Title

Signaling through the adaptor molecule MyD88 in CD4+ T cells is required to overcome suppression by regulatory T cells.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE26460
Expression data from primary hepatocytes isolated from miR-143DOX mice
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

The contribution of altered posttranscriptional gene silencing (PTGS) to the development of insulin resistance and type 2 diabetes mellitus so far remains elusive. We have described that expression of microRNAs (miR)-143 and -145 is dysregulated in genetic and dietary mouse models of obesity. Induced transgenic overexpression of miR-143, but not miR-145, causes insulin resistance and impaired insulin-stimulated AKT activation. We used microarrays to analyze the underlying molecular mechanisms of miR-143-mediated development of insulin resistance.

Publication Title

Obesity-induced overexpression of miRNA-143 inhibits insulin-stimulated AKT activation and impairs glucose metabolism.

Sample Metadata Fields

Specimen part, Treatment

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accession-icon SRP110814
Hepatic Expression of Ectodysplasin (ED) A Increases in Obesity and Impairs Insulin Sensitivity in Skeletal Muscle
  • organism-icon Mus musculus
  • sample-icon 8 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 4000

Description

We screened intronic microRNAs dysregulated in liver of obese mouse models to identify previously uncharacterized coding host genes that may contribute to the pathogenesis of obesity-associated insulin resistance and type 2 diabetes mellitus. Our approach identified the expression of Ectodysplasin A (Eda), the causal gene of X-linked hypohidrotic ectodermal dysplasia (XLHED; MIM 305100) was strongly increased in liver of obese mouse models both in rodents and humans.Eda expression in murine liver is controlled via PPAR? activation, increases in circulation and promotes JNK activation and inhibitory serine phosphorylation of IRS1 in skeletal muscle. Consistently, bi-directional modulation of hepatic Eda expression in mouse models affects systemic glucose metabolism with alterations of muscle insulin signaling, revealing a novel role of EDA as an obesity-associated hepatokine, which impairs insulin sensitivity in skeletal muscle. Overall design: Soleus muscle mRNA profiles of db/db mice at 3 weeks after injection of AAV encoding shRNA targeting mouse Eda or the control scrambled shRNA sequence at the titer of 2-3x10e10 particles/body.

Publication Title

A microRNA screen reveals that elevated hepatic ectodysplasin A expression contributes to obesity-induced insulin resistance in skeletal muscle.

Sample Metadata Fields

Age, Specimen part, Subject

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accession-icon GSE42188
Adenoviral shRNA-based knockdown of hepatic Hnf1b (Ad-shHnf1b)
  • organism-icon Mus musculus
  • sample-icon 7 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

Insulin resistance represents a hallmark during the development of type 2 diabetes mellitus (T2D) and in the pathogenesis of obesity-associated disturbances of glucose and lipid metabolism 1,2,3. MicroRNA (miR)-dependent posttranscriptional gene silencing has recently been recognized to control gene expression in disease development and progression including that of insulin-resistant T2D. MiRs, whose deregulation alters hepatic insulin sensitivity include miR-143, miR-181 and miR-103/107. Here we report that expression of miR-802 is increased in liver of two obese mouse models and of obese human subjects. Inducible transgenic overexpression of miR-802 in mice causes impaired glucose tolerance and attenuates insulin sensitivity, while reduction of miR-802 expression improves glucose tolerance and insulin action. We identify Hnf1b as a target of miR-802-dependent silencing and shRNA-mediated reduction of Hnf1b in liver causes glucose intolerance, impairs insulin signaling and promotes hepatic gluconeogenesis. In turn, hepatic overexpression of Hnf1b improves insulin sensitivity in db/db mice. Thus, the present study defines a critical role for deregulated expression of miR-802 in the development of obesity-associated impairment of glucose metabolism via targeting Hnf1b and assigns Hnf1b an unexpected role in the control of hepatic insulin sensitivity.

Publication Title

Obesity-induced overexpression of miR-802 impairs glucose metabolism through silencing of Hnf1b.

Sample Metadata Fields

Sex, Specimen part

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accession-icon GSE30762
Mouse expression analysis
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

Comparison between APPPS1-FVB and APPPS1-FVBxABCC1ko mice

Publication Title

Cerebral amyloid-β proteostasis is regulated by the membrane transport protein ABCC1 in mice.

Sample Metadata Fields

Specimen part

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accession-icon GSE47426
Expression Data from murine control and IL6ralpha-deficient macrophages stimulated with Interleukin-6
  • organism-icon Mus musculus
  • sample-icon 8 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

IL-6 induces IL4ralpha expression in macrophages. This mechanism is necessary to promote macrophage polarization towards an M2-phenotype and is crucial to limit the inflammatory response both upon obesity and LPS-endotoxemia.

Publication Title

Signaling by IL-6 promotes alternative activation of macrophages to limit endotoxemia and obesity-associated resistance to insulin.

Sample Metadata Fields

Specimen part

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accession-icon SRP081104
Olfactory sensory neuron-specific IGF1R knockout in mice results in increased smell perception, insulin resistance and adiposity
  • organism-icon Mus musculus
  • sample-icon 8 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

Olfaction is fundamental for survival but there is little known about the connection between smell perception and metabolism. In this study we implemented IGF1R knockout mice in the olfactory sensory neurons, by olfactory marker protetin (OMP) Cre specific recombination, and investigated metabolic parameters, smell perception and transcriptome sequencing. We could demonstrate that IGF1R knockout in the olfactory sensory neurons results in enhanced smell perception, insulin resistance under normal chow diet conditions and increased adiposity in mice fed control diet. Transcriptome analysis of the olfactory epithelium revealed differential expression of markers for mature and immature olfactory sensory neurons, being down-regulated and up- regulated respectively, pointing to differentiation-dependent changes that result in increased olfactory perception. Collectively, this study provides evidence that enhanced smell perception can result in insulin resistance and increased adiposity. Overall design: mRNA profiles of olfactory sensory neurons (OSN) extracted from homozygous tissue-specific IGF1R knockout (OMPIGF1R) and respective cotnrol mice (OMPflfl) were generated by deep sequencing, in four replicates using Illumina sequencing

Publication Title

The Sense of Smell Impacts Metabolic Health and Obesity.

Sample Metadata Fields

Age, Cell line, Subject

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accession-icon GSE56989
Genome-wide identification of HIF-1 and HIF-2 binding sites in hypoxic human macrophages alternatively activated by IL-10
  • organism-icon Homo sapiens
  • sample-icon 36 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

Primary human macrophages with a HIF-1alpha or HIF-2alpha knockdown were pretreated with IL-10 for 16h and afterwards for 4h additionaly under hypoxi (1% O2), RNA was isolated usind the Qiagen RNAeasy Kit and cDNA synthesis wos done using Ambion WT Expression Kit. Expression was compared to si control under control conditions.

Publication Title

Genome-wide identification of hypoxia-inducible factor-1 and -2 binding sites in hypoxic human macrophages alternatively activated by IL-10.

Sample Metadata Fields

Specimen part

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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