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accession-icon GSE52721
Effects of O-GlcNAc modification on gene expression using O-GlcNAcase deleted Mouse Embryonic Fibroblast cells.
  • organism-icon Mus musculus
  • sample-icon 9 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Single O-GlcNAc modification orchestrate by O-GlcNAc Transferase (OGT) and O-GlcNAcase (OGA alias MGEA5) enzymes, affects signal transduction and gene expression by chromatin modulation. We developed Oga deleted MEF (mouse embryonic fibroblast) cells to investigate effects of O-GlcNAc modification in mice. RNA isolated from Mouse Embryonic Fibroblast cells generated from Oga Knock out (KO) Heterozygous (Het) and wild type (WT) cells and subjected to microarray analysis.

Publication Title

Conditional knock-out reveals a requirement for O-linked N-Acetylglucosaminase (O-GlcNAcase) in metabolic homeostasis.

Alternate Accession IDs

E-GEOD-52721

Sample Metadata Fields

Sex, Specimen part

View Samples
accession-icon GSE16263
PTIP-regulated genes in MEF
  • organism-icon Mus musculus
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

PPARg and C/EBPa cooperate to control preadipocyte differentiation (adipogenesis). However, the factors that regulate PPARg and C/EBPa expression during adipogenesis remain largely unclear. Here we show PTIP, a protein that associates with histone H3K4 methyltransferases, regulates PPARg and C/EBPa expression in mouse embryonic fibroblasts (MEFs) and during preadipocyte differentiation. PTIP deletion in MEFs leads to marked decreases of PPARg expression and PPARg-stimulated C/EBP expression. Further, PTIP is essential for induction of PPARg and C/EBPa expression during preadipocyte differentiation. Deletion of PTIP impairs the enrichment of H3K4 trimethylation and RNA polymerase II on PPARg and C/EBPa promoters. Accordingly, PTIP-/- MEFs and preadipocytes all show striking defects in adipogenesis. Furthermore, rescue of the adipogenesis defect in PTIP-/- MEFs requires co-expression of PPARg and C/EBPa. Finally, deletion of PTIP in brown adipose tissue significantly reduces tissue weight in mice. Thus, by regulating PPARg and C/EBPa expression, PTIP plays a critical role in adipogenesis.

Publication Title

Histone methylation regulator PTIP is required for PPARgamma and C/EBPalpha expression and adipogenesis.

Alternate Accession IDs

E-GEOD-16263

Sample Metadata Fields

Cell line

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accession-icon GSE6795
Expression data from C57BL6 tissues and 3T3-L1 fibroblasts
  • organism-icon Mus musculus
  • sample-icon 28 Downloadable Samples
  • Technology Badge Icon Affymetrix Murine 11K SubA Array (mu11ksuba)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Xanthine oxidoreductase is a regulator of adipogenesis and PPARgamma activity.

Alternate Accession IDs

E-GEOD-6795

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE6794
Expression data from 3T3-L1 adipogenesis
  • organism-icon Mus musculus
  • sample-icon 18 Downloadable Samples
  • Technology Badge Icon Affymetrix Murine 11K SubA Array (mu11ksuba)

Description

3T3-L1 fibroblasts are a commonly used in vitro model for adipogenesis. When induced with hormones, they differentiate into mature fat cells. Here, microarrays were used to study 3T3-L1 adipose differentiation through time.

Publication Title

Xanthine oxidoreductase is a regulator of adipogenesis and PPARgamma activity.

Alternate Accession IDs

E-GEOD-6794

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon GSE73131
Sphingosine-1-phosphate Phosphatase 2 Regulates Pancreatic Islet -cell Endoplasmic Reticulum Stress and Proliferation
  • organism-icon Mus musculus
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Sphingosine-1-phosphate (S1P) is a sphingolipid metabolite that regulates basic cell functions through metabolic and signaling pathways. Intracellular metabolism of S1P is controlled, in part, by two homologous S1P phosphatases, 1 and 2, which are encoded by Sgpp1 and Sgpp2, respectively. S1P phosphatase activity is needed for efficient recycling of sphingosine into the sphingolipid synthesis pathway. S1P phosphatase 1 is important for skin homeostasis, but little is known about the functional role of S1P phosphatase 2. To identify the functions of S1P phosphatase 2 in vivo, we studied mice with the Sgpp2 gene deleted. In contrast to Sgpp1-/- mice, Sgpp2-/- mice had normal skin and were viable into adulthood. Unexpectedly, WT mice expressed Sgpp2 mRNA at high levels in pancreatic islets when compared with other tissues. Sgpp2-/- mice had normal blood insulin levels and pancreatic islet size; however, Sgpp2-/- mice treated with a high-fat diet (HFD) had significantly lower blood insulin levels and smaller pancreatic islets compared with WT mice. The smaller islets in the HFD-treated Sgpp2-/- mice had a significantly lower adaptive -cell proliferation rate in response to the diet compared with HFD-treated WT mice. Importantly, -cells from Sgpp2-/- mice fed a normal diet showed significantly increased expression of proteins characteristic of the endoplasmic reticulum (ER) stress response compared with -cells from WT mice. Our results suggest that Sgpp2 deletion causes -cell ER stress, which is a known cause of -cell dysfunction, and reveal a novel juncture in the sphingolipid recycling pathway that could impact the development of diabetes.

Publication Title

Sphingosine-1-phosphate Phosphatase 2 Regulates Pancreatic Islet β-Cell Endoplasmic Reticulum Stress and Proliferation.

Alternate Accession IDs

E-GEOD-73131

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon GSE6793
Expression data from select tissues harvested from C57BL6 mice
  • organism-icon Mus musculus
  • sample-icon 10 Downloadable Samples
  • Technology Badge Icon Affymetrix Murine 11K SubA Array (mu11ksuba)

Description

Gene expression was studied from different mouse tissues

Publication Title

Xanthine oxidoreductase is a regulator of adipogenesis and PPARgamma activity.

Alternate Accession IDs

E-GEOD-6793

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon GSE21746
Mus musculus intestine
  • organism-icon Mus musculus
  • sample-icon 2 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

A tissue-specific landscape of sense/antisense transcription in the mouse intestine.

Alternate Accession IDs

E-GEOD-21746

Sample Metadata Fields

Specimen part

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accession-icon GSE19767
Microarray expression data from the Mus musculus intestine
  • organism-icon Mus musculus
  • sample-icon 2 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Genome wide expression profiling to determine the overlap of Affymetrix-signals with SOLID sequencing

Publication Title

A tissue-specific landscape of sense/antisense transcription in the mouse intestine.

Alternate Accession IDs

E-GEOD-19767

Sample Metadata Fields

Specimen part

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accession-icon SRP094473
A neural basis for melanocortin-4 receptor-regulated appetite.
  • organism-icon Mus musculus
  • sample-icon 63 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

Pro-opiomelanocortin (POMC)- and agouti-related peptide (AgRP)-expressing neurons of the arcuate nucleus of the hypothalamus (ARC) are oppositely regulated by caloric depletion and coordinately stimulate and inhibit homeostatic satiety, respectively. This bimodality is principally underscored by the antagonistic actions of these ligands at downstream melanocortin-4 receptors (MC4R) in the paraventricular nucleus of the hypothalamus (PVH). Although this population is critical to energy balance, the underlying neural circuitry remains unknown. Using mice expressing Cre recombinase in MC4R neurons, we demonstrate bidirectional control of feeding following real-time activation and inhibition of PVH(MC4R) neurons and further identify these cells as a functional exponent of ARC(AgRP) neuron-driven hunger. Moreover, we reveal this function to be mediated by a PVH(MC4R)?lateral parabrachial nucleus (LPBN) pathway. Activation of this circuit encodes positive valence, but only in calorically depleted mice. Thus, the satiating and appetitive nature of PVH(MC4R)?LPBN neurons supports the principles of drive reduction and highlights this circuit as a promising target for antiobesity drug development. Overall design: Single-neuron mRNA-seq was performed on fluorescently-labeled or -unlabeled cells that were manually isolated from dissociated adult mouse paraventricular and arcuate hypothalamus: Mc4r-2a-Cre::L10-GFP+ or Mc4r-2a-Cre::AAV-XFP+ or Mc4r-2a-Cre::AAV-XFP-negative PVH neurons; Agrp-IRES-Cre::L10-GFP+ ARC neurons; Pomc-hrGFP+ ARC neurons; and vGLUT2-IRES-Cre::AAV-XFP+ ARC neurons Note: Raw files unavailable for samples GSM2413312 GSM2413313 GSM2413314 GSM2413346 GSM2413347

Publication Title

A neural basis for melanocortin-4 receptor-regulated appetite.

Alternate Accession IDs

GSE90809

Sample Metadata Fields

Sex, Specimen part, Cell line, Subject

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accession-icon GSE28598
Protection from obesity and diabetes by blockade of TGF-beta/Smad3 signaling
  • organism-icon Mus musculus
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Imbalances in glucose and energy homeostasis are at the core of the worldwide epidemic of obesity and diabetes. Here, we illustrate an important role of the TGF-beta/Smad3 signaling pathway in regulating glucose and energy homeostasis. Smad3 deficient mice are protected from diet-induced obesity and diabetes. Interestingly, the metabolic protection is accompanied by Smad3-/- white adipose tissue acquiring the bioenergetic and gene expression profile of brown fat/skeletal muscle. Smad3-/- adipocytes demonstrate a marked increase in mitochondrial biogenesis, with a corresponding increase in basal respiration, and Smad3 acts as a repressor of PGC-alpha1 expression. We observe significant correlation between TGF-beta1 levels and adiposity in rodents and humans. Further, systemic blockade of TGF-beta1 signaling protects mice from obesity, diabetes and hepatic steatosis. Together, these results demonstrate that TGF-beta signaling regulates glucose tolerance and energy homeostasis and suggest that modulation of TGF-beta1 activity might be an effective treatment strategy for obesity and diabetes.

Publication Title

Protection from obesity and diabetes by blockade of TGF-β/Smad3 signaling.

Alternate Accession IDs

E-GEOD-28598

Sample Metadata Fields

Treatment

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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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