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accession-icon GSE134282
The role of methyl-CpG-binding domain protein-2 (MBD2) in colonic inflammation
  • organism-icon Mus musculus
  • sample-icon 45 Downloadable Samples
  • Technology Badge IconIllumina MouseWG-6 v2.0 expression beadchip

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

The Methyl-CpG-Binding Protein Mbd2 Regulates Susceptibility to Experimental Colitis via Control of CD11c<sup>+</sup> Cells and Colonic Epithelium.

Sample Metadata Fields

Specimen part

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accession-icon GSE134280
The role of methyl-CpG-binding domain protein-2 (MBD2) in colonic inflammation [series 1]
  • organism-icon Mus musculus
  • sample-icon 27 Downloadable Samples
  • Technology Badge IconIllumina MouseWG-6 v2.0 expression beadchip

Description

Mice deficient in MBD2 (Mbd2-/-) were treated with 2% dextran sulfate sodium or normal drinking water for 6 continuous days. A single cell suspension of colon lamina propria and epithelium was isolated, with monocytes (CD11b+ Ly6CHi, MHC-II+/-), macrophages (CD11b+ Ly6C-MHC-II+), cDC2s (CD11b- CD11c+ CD103+) and epithelial cells (CD45- EpCAM+) purified by FACS.

Publication Title

The Methyl-CpG-Binding Protein Mbd2 Regulates Susceptibility to Experimental Colitis via Control of CD11c<sup>+</sup> Cells and Colonic Epithelium.

Sample Metadata Fields

Specimen part

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accession-icon GSE134281
The role of methyl-CpG-binding domain protein-2 (MBD2) in colonic inflammation [series 2]
  • organism-icon Mus musculus
  • sample-icon 18 Downloadable Samples
  • Technology Badge IconIllumina MouseWG-6 v2.0 expression beadchip

Description

Mice deficient in MBD2 (Mbd2-/-) were treated with 2% dextran sulfate sodium or normal drinking water for 6 continuous days. A single cell suspension of colon lamina propria and epithelium was isolated, with monocytes (CD11b+ Ly6CHi, MHC-II+/-), macrophages (CD11b+ Ly6C-MHC-II+), cDC2s (CD11b- CD11c+ CD103+) and epithelial cells (CD45- EpCAM+) purified by FACS.

Publication Title

The Methyl-CpG-Binding Protein Mbd2 Regulates Susceptibility to Experimental Colitis via Control of CD11c<sup>+</sup> Cells and Colonic Epithelium.

Sample Metadata Fields

Specimen part

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accession-icon GSE12304
Albumin, TGF-Beta1 and Blood-Brain Barrier opening induce cortical epileptogenesis.
  • organism-icon Rattus norvegicus
  • sample-icon 19 Downloadable Samples
  • Technology Badge Icon Affymetrix Rat Genome 230 2.0 Array (rat2302)

Description

Insults to the cerebral cortex, such as trauma, ischemia or infections, may result in the development of epilepsy, one of the most common neurological disorders. Previous studies have suggested that perturbations in neurovascular integrity and breakdown of the blood-brain barrier (BBB) lead to neuronal hypersynchronization and epileptiform activity, but the underlying mechanisms are unknown. As with BBB opening, treatment with albumin or with TGF-1 results in the development of hypersynchronized epileptiform activity. Given the latent period before the appearance of epileptiform activity, we hypothesized the underlying mechanism is a transcriptional response which would be similar for BBB breakdown and exposure to albumin or TGF-1. In search of a common pathway and transcriptional activation pattern we performed a genome wide analysis. Genomic expression analyses demonstrated similar expression patterns for BBB opening, albumin and TGF-1 exposure. Most importantly, TGF- pathway blockers suppressed most albumin-induced transcriptional changes.

Publication Title

Astrocytic dysfunction in epileptogenesis: consequence of altered potassium and glutamate homeostasis?

Sample Metadata Fields

Sex

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accession-icon SRP028609
Small RNA content in mouse serum upon S.mansoni infection
  • organism-icon Mus musculus
  • sample-icon 4 Downloadable Samples
  • Technology Badge IconIllumina Genome Analyzer IIx, Illumina HiSeq 2000

Description

MicroRNAs (miRNAs) are a class of short non-coding RNA that play important roles in disease processes in animals and are present in a highly stable cell-free form in body fluids. Here we examine the capacity of host and parasite miRNAs to serve as tissue or serum biomarkers of Schistosoma mansoni infection. Sequencing of small RNAs from serum confirmed the presence of miRNAs and revealed 11 parasite-derived miRNAs that were detectable by 8 weeks post S.mansoni infection. Overall design: Small RNA content in serum of naïve and Schistosoma mansoni infected mice were examined in two different librarys. 1- prepared according to the 290 Illumina small RNA Sample Preparation Kit version 1.5 and sequenced on the GAIIX and 2- prepared according to the TruSeq Small RNA protocol (without size-selecting small 295 RNA) and sequenced on the HiSeq2

Publication Title

Parasite-derived microRNAs in host serum as novel biomarkers of helminth infection.

Sample Metadata Fields

Sex, Cell line, Subject

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accession-icon GSE25504
Whole blood mRNA expression profiling of host molecular networks in neonatal sepsis
  • organism-icon Homo sapiens
  • sample-icon 25 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

We aimed to identify the gene network and pathway biology associated with neonatal sepsis by determining genome-wide alterations in host RNA in infected infants

Publication Title

Identification of a human neonatal immune-metabolic network associated with bacterial infection.

Sample Metadata Fields

Sex, Specimen part

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accession-icon GSE29747
Sporisorium reilianum Infection Changes Inflorescence and Branching Architectures of Maize
  • organism-icon Zea mays
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Maize Genome Array (maize)

Description

S. reilianum triggered loss of organ and meristem identity, and loss of meristem determinacy in male and female inflorescences and flowers. Microarray analysis showed that these developmental changes were accompanied with transcriptional regulation of genes proposed to regulate floral organ and meristem identity, and meristem determinacy in maize.

Publication Title

Sporisorium reilianum infection changes inflorescence and branching architectures of maize.

Sample Metadata Fields

Specimen part, Time

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accession-icon SRP184711
The lung environment controls alveolar macrophage metabolism and responsiveness during type-2 inflammation.
  • organism-icon Mus musculus
  • sample-icon 13 Downloadable Samples
  • Technology Badge IconNextSeq 500

Description

Fine control of macrophage activation is required to prevent inflammatory disease, particularly at barrier sites such as the lung. However, the dominant mechanisms that regulate pulmonary MFs during inflammation are currently poorly understood. Here we show that airway MFs are substantially less able to respond to the canonical type-2 cytokine IL-4, which underpins allergic disease and parasite worm infections, than lung tissue or peritoneal cavity MFs. We reveal that MF hypo-responsiveness to IL-4 is dictated by the lung environment, though independent of the host microbiota or the prominent lung extracellular matrix components surfactant protein D and mucin 5b. Rather, compared to cavity MFs,  airway MFs display severely dysregulated metabolism. Strikingly, upon removal from the lung, alveolar MFs regain IL-4 responsiveness in a process dependent upon glycolysis. Thus, we propose that impaired glycolysis within the pulmonary niche is a central determinant for regulation of MF responsiveness during type-2 inflammation. Overall design: The 13 analysed samples belong to 6 different groups, each group consisted of 2 or 3 samples. The groups consist of 3 separate macrophage populations, from either control or IL-4 complex treated mice. Each individual sample was generated from 3-5 pooled biological replicate mice.

Publication Title

The lung environment controls alveolar macrophage metabolism and responsiveness in type 2 inflammation.

Sample Metadata Fields

Treatment, Subject

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accession-icon GSE34053
CD133+ colon cancer cells are more interactive with the tumor microenvironment than CD133- cells
  • organism-icon Homo sapiens
  • sample-icon 8 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

CD133-positive colorectal cancer cells exhibit enhanced tumorigenicity over CD133-negative cells. The CD133+ cells are more interactive with and responsive to their stromal microenvironment because they also express the cognate receptors, such as CXCR4, for ligands produced by their neighboring carcinoma-associated fibroblasts, such as SDF-1 (stromal-derived growth factor).

Publication Title

CD133+ colon cancer cells are more interactive with the tumor microenvironment than CD133- cells.

Sample Metadata Fields

Specimen part, Disease, Disease stage

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accession-icon GSE7823
Murine Pulmonary Response to Chronic Hypoxia is Strain Specific
  • organism-icon Mus musculus
  • sample-icon 9 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

6-8 week old BL6, FVB/N and SV129 mouse strains were kept in normoxia or hypobaric hypoxia for 4 weeks and then phenotyped by echocardiogram and right ventricular heart catheterization, followed by tissue collection. In addition, Affymetrix expression analysis was conducted in a paired fashion.

Publication Title

Murine pulmonary response to chronic hypoxia is strain specific.

Sample Metadata Fields

No sample metadata fields

View Samples

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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