refine.bio
  • Search
      • Normalized Compendia
      • RNA-seq Sample Compendia
  • Docs
  • About
  • My Dataset
github link
Showing
of 22 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 GSE13335
Gene expression analysis of cells sensitive to necrosis (L929) and cells sensitive to apoptosis (NIH3T3).
  • organism-icon Mus musculus
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon

Description

To explore gene expression profiles of cells sensitive to necrosis (such as L929 cells) and those sensitive to apoptosis (such as NIH3T3 cells), we conducted expression microarray analysis of L929 cells and NIH3T3 cells.

Publication Title

Identification of a molecular signaling network that regulates a cellular necrotic cell death pathway.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon GSE12982
Expression data from mouse ES cells and various differentiated cell types
  • organism-icon Mus musculus
  • sample-icon 53 Downloadable Samples
  • Technology Badge Icon

Description

We used microarrays to detail the role of Polycomb proteins including Ezh2 and Eed in maintaining ES cell identity and executing pluripotency.

Publication Title

EZH1 mediates methylation on histone H3 lysine 27 and complements EZH2 in maintaining stem cell identity and executing pluripotency.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon GSE27083
Expression data from MMTV-PDK1 transgenic mice
  • organism-icon Mus musculus
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon

Description

The role of PDK1 on mammary tumorigenesis and its interaction with PPARdelta, was assessed. Transgenic mice were generated in which PDK1 was expressed in the mammary epithelium.

Publication Title

PPARδ activation acts cooperatively with 3-phosphoinositide-dependent protein kinase-1 to enhance mammary tumorigenesis.

Sample Metadata Fields

Specimen part, Treatment

View Samples
accession-icon GSE19169
Jumonji modulates Polycomb activity and self-renewal versus differentiation of stem cells
  • organism-icon Mus musculus
  • sample-icon 30 Downloadable Samples
  • Technology Badge Icon

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Jumonji modulates polycomb activity and self-renewal versus differentiation of stem cells.

Sample Metadata Fields

Specimen part

View Samples
accession-icon GSE19165
Microarray profiling analysis in Jmj-Fl/Fl and Jmj-null ESCs.
  • organism-icon Mus musculus
  • sample-icon 30 Downloadable Samples
  • Technology Badge Icon

Description

We used microarrays to detail the role of JMJ in ES cell function.

Publication Title

Jumonji modulates polycomb activity and self-renewal versus differentiation of stem cells.

Sample Metadata Fields

Specimen part

View Samples
accession-icon GSE16067
Gene expression analysis in control and HIF-2 alpha deficient murine lung endothelial cells under hypoxia
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon

Description

Journal : Blood. 2009 Jul 9;114(2):469-77. Epub 2009 May 13.

Publication Title

Endothelial deletion of hypoxia-inducible factor-2alpha (HIF-2alpha) alters vascular function and tumor angiogenesis.

Sample Metadata Fields

Specimen part

View Samples
accession-icon GSE35181
beta-Arrestin Pathway-Selective G Protein-Coupled Receptor Agonists Engender Unique Biological Efficacy In Vivo
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon

Description

Biased GPCR agonists are orthosteric ligands that possess pathway-selective efficacy, activating or inhibiting only a subset of the signaling repertoire of their cognate receptors. In vitro, D-Trp12,Tyr34-bPTH(7-34) (PTH-{beta}arr), a biased agonist for the type 1 parathyroid hormone receptor, antagonizes receptor-G protein coupling but activates arrestin-dependent signaling. In vivo, both PTH-{beta}arr and the conventional agonist PTH(1-34) stimulate anabolic bone formation. To understand how two PTH1R ligands with markedly different in vitro efficacy could elicit similar in vivo responses, we analyzed transcriptional profiles from calvarial bone of mice treated for 8 weeks with vehicle, PTH-{beta}arr or PTH(1-34). Treatment of wild type mice with PTH-{beta}arr primarily affected pathways that promote expansion of the osteoblast pool, notably cell cycle regulation, cell survival and migration. These responses were absent in beta-arrestin2 null mice, identifying them as downstream targets of beta-arrestin2-mediated signaling. In contrast, PTH(1-34) primarily affected pathways classically associated with enhanced bone formation, including collagen synthesis and matrix mineralization. PTH(1-34) actions were less dependent on beta-arrestin2, as might be expected of a ligand capable of G protein activation. These results illustrate the uniqueness of biased agonism in vivo and demonstrate that functional selectivity can be exploited to change the quality of GPCR efficacy.

Publication Title

β-arrestin-selective G protein-coupled receptor agonists engender unique biological efficacy in vivo.

Sample Metadata Fields

Specimen part, Treatment

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

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