refine.bio
  • Search
      • Normalized Compendia
      • RNA-seq Sample Compendia
  • Docs
  • About
  • My Dataset
github link
Showing
of 13 results
Sort by

Filters

Technology

Platform

accession-icon GSE21056
Differential roles of Sall4 isoforms in ES cell pluripotency
  • organism-icon Mus musculus
  • sample-icon 8 Downloadable Samples
  • Technology Badge Icon

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Differential roles of Sall4 isoforms in embryonic stem cell pluripotency.

Sample Metadata Fields

Specimen part, Cell line

View Samples
accession-icon GSE21054
Differential roles of Sall4 isoforms in ES cell pluripotency: expression
  • organism-icon Mus musculus
  • sample-icon 8 Downloadable Samples
  • Technology Badge Icon

Description

Murine embryonic stem cells (ESCs) are defined by continuous self-renewal and pluripotency. A diverse repertoire of protein isoforms arising from alternative splicing are expressed in ES cells without defined biological roles. Sall4, a transcription factor essential for pluripotency, exists as two isoforms (Sall4a and Sall4b). By genome-wide location analysis, we have determined that Sall4b, and not Sall4a, binds preferentially to highly expressed loci in ES cells. Sall4a and Sall4b binding sites are distinguished by both epigenetic marks at target loci and their clustering with binding sites of other pluripotency factors. When ESCs expressing a single isoform of Sall4 are generated, Sall4b alone could maintain the pluripotent state, although it could not completely suppress all differentiation markers. Sall4a and Sall4b collaborate in maintenance of the pluripotent state, but play distinct roles. Our work is novel in establishing such isoform-specific differences in ES cells.

Publication Title

Differential roles of Sall4 isoforms in embryonic stem cell pluripotency.

Sample Metadata Fields

Specimen part, Cell line

View Samples
accession-icon GSE63325
The cohesin associated factor Wapal is required for proper polycomb-mediated gene silencing
  • organism-icon Mus musculus
  • sample-icon 10 Downloadable Samples
  • Technology Badge Icon

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

The cohesin-associated protein Wapal is required for proper Polycomb-mediated gene silencing.

Sample Metadata Fields

Specimen part

View Samples
accession-icon GSE63291
The cohesin offloading factor Wapal is required for proper polycomb-mediated gene silencing [array]
  • organism-icon Mus musculus
  • sample-icon 10 Downloadable Samples
  • Technology Badge Icon

Description

The cohesin offloading protein Wapal also acts as a polycomb factor in flies. We examined its role in transcriptional role in murine embryonic stem cells (ESCs)

Publication Title

The cohesin-associated protein Wapal is required for proper Polycomb-mediated gene silencing.

Sample Metadata Fields

Specimen part

View Samples
accession-icon GSE38409
Expression data from mouse lungs, exposed in-utero to second-hand smoke (SHS) and challenged with ovalbumin (OVA) as adults.
  • organism-icon Mus musculus
  • sample-icon 15 Downloadable Samples
  • Technology Badge Icon

Description

SHS exposure during pregnancy has adverse effects on offspring.

Publication Title

In utero exposure to second-hand smoke aggravates the response to ovalbumin in adult mice.

Sample Metadata Fields

Sex, Specimen part

View Samples
accession-icon GSE54774
Expression data from mice on a high fat, high carbohydrate diet treated with exenatide
  • organism-icon Mus musculus
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon

Description

The present study was constructed to confirm previous findings that mice on a high fat diet (HFD) treated by subcutaneous injection with exenatide (EXE) at 3g/kg once daily for 6 weeks develop exocrine pancreatic injury (Rouse et al. 2014). The present study included 12 weeks of EXE exposure at multiple concentrations (3, 10, or 30 g/kg) with multiple endpoints (histopathology evaluations, immunoassay for cytokines, immunostaining of the pancreas, serum chemistries and measurement of trypsin, amylase, and, lipase, and gene expression profiles). Time- and dose-dependent exocrine pancreatic injury was observed in mice associated with EXE exposure in a HFD environment. The time- and dose-dependent morphological changes identified in the pancreas involved acinar cell injury and death (autophagy, apoptosis, necrosis, and atrophy), cell adaptations (hypertrophy and hyperplasia), and cell survival (regeneration) accompanied with varying degrees of inflammatory response leading to secondary injury in pancreatic blood vessels, ducts, and adipose tissues. Gene expression profiles supported the presence of increased signaling for cell survival and altered lipid metabolism. The potential for EXE to cause acute or early chronic pancreatic injury was identified in a HFD environment. In human disease, the influence of pancreatitis risk factors or pre-existing chronic pancreatitis on this injury potential requires further investigation.

Publication Title

Extended exenatide administration enhances lipid metabolism and exacerbates pancreatic injury in mice on a high fat, high carbohydrate diet.

Sample Metadata Fields

Sex, Specimen part

View Samples
accession-icon GSE87081
Functional Roles of Acetylated Histone Marks at Mouse Meiotic Recombination Hotspots
  • organism-icon Mus musculus
  • sample-icon 23 Downloadable Samples
  • Technology Badge Icon

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Functional Roles of Acetylated Histone Marks at Mouse Meiotic Recombination Hot Spots.

Sample Metadata Fields

Sex, Age, Specimen part

View Samples
accession-icon GSE25825
Expression data from MxCre;E2F1-/-2-/-3f/f Cd11B myeloid cells
  • organism-icon Mus musculus
  • sample-icon 5 Downloadable Samples
  • Technology Badge Icon

Description

To understand the underlying cause for the observed apoptosis in E2f1-3 deficient myeloid cells. We compared gene expression profiles of Cd11b+ sorted myeloid cells isolated from bone marrow of control (E2F1-/- ) and experimental (Mxcre;E2F1-/-2-/-3f/f ) mice.

Publication Title

E2f1-3 are critical for myeloid development.

Sample Metadata Fields

Age, Specimen part

View Samples
accession-icon GSE23641
Expression data of wild type and miR-155 knockout bone marrow derived dendritic cells treated with lipopolysaccharide (LPS)
  • organism-icon Mus musculus
  • sample-icon 2 Downloadable Samples
  • Technology Badge Icon

Description

We used microarrays to look at overall gene expression differences between miR-155-/- and WT dendritic cells under inflammatory conditions.

Publication Title

MicroRNA-155 promotes autoimmune inflammation by enhancing inflammatory T cell development.

Sample Metadata Fields

Specimen part

View Samples
accession-icon GSE33201
A mouse model of the most aggressive subgroup of human medulloblastoma
  • organism-icon Mus musculus
  • sample-icon 64 Downloadable Samples
  • Technology Badge Icon

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

A mouse model of the most aggressive subgroup of human medulloblastoma.

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)

fund-icon Fund the CCDL

Developed by the Childhood Cancer Data Lab

Powered by Alex's Lemonade Stand Foundation

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.

BSD 3-Clause LicensePrivacyTerms of UseContact