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accession-icon GSE41257
Transcriptional changes in intraepithelial CD4 lymphocytes
  • organism-icon Mus musculus
  • sample-icon 2 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

We investigated transcriptional changes in CD4CD8aa and CD4 intraepthelial lymphocytes.

Publication Title

Transcriptional reprogramming of mature CD4⁺ helper T cells generates distinct MHC class II-restricted cytotoxic T lymphocytes.

Sample Metadata Fields

Specimen part

View Samples
accession-icon GSE2952
Adipose tissue gene expression profiles of lean, insulin resistant, obese, and diabetic mice.
  • organism-icon Mus musculus
  • sample-icon 20 Downloadable Samples
  • Technology Badge Icon Affymetrix Murine 11K SubA Array (mu11ksuba)

Description

The expression of adipogenic genes is decreased in obesity and diabetes mellitus

Publication Title

The expression of adipogenic genes is decreased in obesity and diabetes mellitus.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon GSE2899
Gene Expression Profiles of Nondiabetic and Diabetic Obese Mice--Adipose tissue, Liver, Muscle and Islets
  • organism-icon Mus musculus
  • sample-icon 16 Downloadable Samples
  • Technology Badge Icon Affymetrix Murine Genome U74A Version 2 Array (mgu74av2)

Description

Obesity is a strong risk factor for the development of type 2 diabetes. We have previously reported that in adipose tissue of obese (ob/ob) mice, the expression of adipogenic genes is decreased. When made genetically obese, the BTBR mouse strain is diabetes susceptible and the C57BL/6J (B6) strain is diabetes resistant. We used DNA microarrays and RT-PCR to compare the gene expression in BTBR-ob/ob versus B6-ob/ob mice in adipose tissue, liver, skeletal muscle, and pancreatic islets. Our results show: 1) there is an increased expression of genes involved in inflammation in adipose tissue of diabetic mice; 2) lipogenic gene expression was lower in adipose tissue of diabetes-susceptible mice, and it continued to decrease with the development of diabetes, compared with diabetes-resistant obese mice; 3) hepatic expression of lipogenic enzymes was increased and the hepatic triglyceride content was greatly elevated in diabetes-resistant obese mice; 4) hepatic expression of gluconeogenic genes was suppressed at the prediabetic stage but not at the onset of diabetes; and 5) genes normally not expressed in skeletal muscle and pancreatic islets were expressed in these tissues in the diabetic mice. We propose that increased hepatic lipogenic capacity protects the B6-ob/ob mice from the development of type 2 diabetes. Diabetes 52:688700, 2003

Publication Title

Gene expression profiles of nondiabetic and diabetic obese mice suggest a role of hepatic lipogenic capacity in diabetes susceptibility.

Sample Metadata Fields

Sex, Age

View Samples
accession-icon GSE43798
Microarray of cardiac biventricle from PGC-1a-/-bf/f/MerCre mice
  • organism-icon Mus musculus
  • sample-icon 10 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

The following abstract from the submitted manuscript describes the major findings of this work.

Publication Title

A role for peroxisome proliferator-activated receptor γ coactivator-1 in the control of mitochondrial dynamics during postnatal cardiac growth.

Sample Metadata Fields

Specimen part

View Samples
accession-icon SRP074380
Hepatic gene expression co-regulated by diet-microbiota interactions (19 wk)
  • organism-icon Mus musculus
  • sample-icon 15 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

Abstract: Histones are small proteins that form the core of nucleosomes, around which eukaryotic DNA wraps to ultimately form the highly organized and compressed structure known as chromatin. The N-terminal tails of histones are highly modified, and the modification state of these proteins dictates whether chromatin is permissive or repressive to processes that require physical access to DNA, including transcription and DNA replication and repair. The enzymes that add and remove histone modifications are known to be exquisitely sensitive to endogenous small molecule metabolite availability. In this manner, chromatin can adapt to changes in environment, particularly diet-induced metabolic state. Importantly, gut microbiota contribute to robust host metabolic phenotypes, and produce a myriad of metabolites that are detectable in host circulation. Further, gut microbial community composition and metabolite production are regulated by host diet, as a major source of carbon and energy for the microbiota. While prior studies have reported robust host metabolic associations with gut microbiota, the mechanisms therein remain largely unknown. Here we demonstrate that microbial colonization regulates global histone acetylation and methylation in multiple host tissues including colon, adipose tissue, and liver. This regulatory relationship is altered by diet: a “Western-type” diet leads to a general suppression of the microbiota-dependent chromatin changes observed in a polysaccharide rich diet. Finally, we demonstrate that supplementation of germ-free mice with major products of gut bacterial fermentation (i.e., short-chain fatty acids acetate, propionate, and butyrate) is sufficient to recapitulate many of the effects of colonization on host epigenetic states. These findings have profound implications for understanding the complex functional interactions between diet, gut microbiota, and host health. Overall design: 15 samples in total (biological n=3 per for each of 5 conditions; 19kw old male C57BL/6J mouse liver): (1) GF mouse liver on chow diet, (2) ConvR mouse liver on chow diet, (3) ConvD mouse liver on chow diet, (4) GF mouse liver on HF/HS diet, (5) ConvR mouse liver on HF/HS diet

Publication Title

Diet-Microbiota Interactions Mediate Global Epigenetic Programming in Multiple Host Tissues.

Sample Metadata Fields

Cell line, Subject

View Samples
accession-icon GSE2926
Gene Expression Profiles of Scd1 knockout mice vs wild type mice on chow diet: Liver.
  • organism-icon Mus musculus
  • sample-icon 9 Downloadable Samples
  • Technology Badge Icon Affymetrix Murine Genome U74A Array (mgu74a)

Description

Loss of stearoyl-CoA desaturase-1 function protects mice against adiposity.

Publication Title

Loss of stearoyl-CoA desaturase-1 function protects mice against adiposity.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon SRP074378
Hepatic gene expression co-regulated by diet-microbiota interactions (14 wk)
  • organism-icon Mus musculus
  • sample-icon 9 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

Abstract: Histones are small proteins that form the core of nucleosomes, around which eukaryotic DNA wraps to ultimately form the highly organized and compressed structure known as chromatin. The N-terminal tails of histones are highly modified, and the modification state of these proteins dictates whether chromatin is permissive or repressive to processes that require physical access to DNA, including transcription and DNA replication and repair. The enzymes that add and remove histone modifications are known to be exquisitely sensitive to endogenous small molecule metabolite availability. In this manner, chromatin can adapt to changes in environment, particularly diet-induced metabolic state. Importantly, gut microbiota contribute to robust host metabolic phenotypes, and produce a myriad of metabolites that are detectable in host circulation. Further, gut microbial community composition and metabolite production are regulated by host diet, as a major source of carbon and energy for the microbiota. While prior studies have reported robust host metabolic associations with gut microbiota, the mechanisms therein remain largely unknown. Here we demonstrate that microbial colonization regulates global histone acetylation and methylation in multiple host tissues including colon, adipose tissue, and liver. This regulatory relationship is altered by diet: a “Western-type” diet leads to a general suppression of the microbiota-dependent chromatin changes observed in a polysaccharide rich diet. Finally, we demonstrate that supplementation of germ-free mice with major products of gut bacterial fermentation (i.e., short-chain fatty acids acetate, propionate, and butyrate) is sufficient to recapitulate many of the effects of colonization on host epigenetic states. These findings have profound implications for understanding the complex functional interactions between diet, gut microbiota, and host health. Overall design: 9 samples in total (biological n=3 per for each of 3 conditions; 14kw old male C57BL/6J mouse liver): (1) GF mouse liver on chow diet, (2) ConvD mouse liver on chow diet, (3) GF mouse liver on chow diet + supplemented drinking water with short chain fatty acids

Publication Title

Diet-Microbiota Interactions Mediate Global Epigenetic Programming in Multiple Host Tissues.

Sample Metadata Fields

Cell line, Subject

View Samples
accession-icon GSE18737
Epigenetic chromatin states uniquely define the developmental plasticity of murine hematopoietic stem cells
  • organism-icon Mus musculus
  • sample-icon 12 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

Epigenetic chromatin states uniquely define the developmental plasticity of murine hematopoietic stem cells.

Sample Metadata Fields

Specimen part

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accession-icon GSE18669
Analysis of murine hematopoieitic stem cells, multipotent progenitors, PreMegE progenitors and mature CD4+ T cells
  • organism-icon Mus musculus
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

An investigation of the global gene expression signatures of murine hematopoietic stem cell differentiation during steady state hematopoiesis.

Publication Title

Epigenetic chromatin states uniquely define the developmental plasticity of murine hematopoietic stem cells.

Sample Metadata Fields

Specimen part

View Samples
accession-icon GSE12750
E. coli K-12 10 uM 5-fluorouracil biofilm vs. E. coli K-12 DMF biofilm
  • organism-icon Escherichia coli
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon Affymetrix E. coli Genome 2.0 Array (ecoli2)

Description

E. coli K-12 ATCC 25404 in LB medium with 5-fluorouracil 10 uM biofilm cells relative to E. coli K-12 ATCC 25404 in LB DMF biofilm cells. The same amount of stock 5-fluoroacil stock solution (0.1% of the volume) was added as DMF into the LB DMF.

Publication Title

5-Fluorouracil reduces biofilm formation in Escherichia coli K-12 through global regulator AriR as an antivirulence compound.

Sample Metadata Fields

No sample metadata fields

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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