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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

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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

View Samples
accession-icon GSE6080
JAM-A Knockdown in HepG2 Cells
  • organism-icon Homo sapiens
  • sample-icon 9 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A 2.0 Array (hgu133a2)

Description

Hepatocytes are polarized epithelial cells whose function depends upon their ability to distinguish between the apical and basolateral surfaces that are located at intercellular tight junctions. It has been proposed that the signaling cascades that originate at these junctions influence cellular activity by controlling gene expression in the cell nucleus. To assess the validity of this proposal with regard to hepatocytes, we depleted expression of the tight junction protein junctional adhesion molecule-A (JAM-A) in the HepG2 human hepatocellular carcinoma cell line. Reduction of JAM-A resulted in a striking change in cell morphology, with cells forming single-layered sheets instead of the normal multi-layered clusters. In the absence of JAM-A, other tight junction proteins were mislocalized, and canaliculi, which form the apical face of the hepatocyte, were consequently absent. While most changes in gene expression were modest, there was a strong transcriptional induction of the adherens junction protein E-cadherin in cells with reduced levels of JAM-A. This increase in E-cadherin was partially responsible for the observed alterations in cell morphology and mislocalization of tight junction proteins. We therefore propose that we have uncovered a novel mechanism for crosstalk between specific components of tight and adherens junctions that can be utilized to regulate adhesion between hepatic cells and to maintain hepatocyte cell polarity.

Publication Title

Junctional adhesion molecule-A is critical for the formation of pseudocanaliculi and modulates E-cadherin expression in hepatic cells.

Sample Metadata Fields

No sample metadata fields

View Samples
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

View Samples
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

View Samples
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

View Samples
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 GSE14414
Gene expression in mouse heart
  • organism-icon Mus musculus
  • sample-icon 15 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

Growth and expansion of ventricular chambers is essential during cardiogenesis and is achieved by proliferation of cardiac progenitors that are not fully differentiated. Disruption of this process can lead to prenatal lethality. In contrast, adult cardiomyocytes achieve growth through hypertrophy rather than hyperplasia. Although epicardial-derived signals may contribute to the proliferative process in myocytes, the factors and cell types responsible for development of the ventricular myocardial thickness are unclear. Moreover, the function of embryonic cardiac fibroblasts, derived from epicardium, and their secreted factors are largely unknown. Using a novel co-culture system, we found that embryonic cardiac fibroblasts induced proliferation of cardiomyocytes, in contrast to adult cardiac fibroblasts that promoted myocyte hypertrophy. We identified fibronectin, collagen and heparin-binding EGF-like growth factor as embryonic cardiac fibroblast-specific signals that collaboratively promoted cardiomyocyte proliferation in a paracrine fashion. b1 integrin was required for this proliferative response, and ventricular cardiomyocyte-specific deletion of b1 integrin in mice resulted in reduced myocardial proliferation and impaired ventricular compaction. These findings reveal a previously unrecognized paracrine function of embryonic cardiac fibroblasts in regulating cardiomyocyte proliferation.

Publication Title

Cardiac fibroblasts regulate myocardial proliferation through beta1 integrin signaling.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE37631
Human Pluripotent Cell Derived Endothelial Cell Characterization
  • organism-icon Homo sapiens
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

Human ES or iPS Cells were differentiated into endothelial cells (ECs) defined by expression of CD31 (PECAM1) and CD144 (VE-Cadherin) on the cell surface. All ES or iPS derived ECs were greater than 90% double positive for these two markers.

Publication Title

Limited gene expression variation in human embryonic stem cell and induced pluripotent stem cell-derived endothelial cells.

Sample Metadata Fields

Specimen part

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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Developed by the Childhood Cancer Data Lab

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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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