refine.bio
  • Search
      • Normalized Compendia
      • RNA-seq Sample Compendia
  • Docs
  • About
  • My Dataset
github link
Showing
of 229 results
Sort by

Filters

Organism

Technology

Platform

accession-icon GSE24369
Gene expression profiling of low-grade fibromyxoid sarcoma (LGFMS)
  • organism-icon Homo sapiens
  • sample-icon 42 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

Analysis of gene expression in 17 low-grade fibromyxoid sarcoma (LGFMS) samples compared to that of histologically similar tumors. LGFMS is characterized by the specific translocations t(7;16)(q33;p11) or t(11;16)(p11;p11) and corresponding fusion genes FUS-CREB3L2 or FUS-CREB3L1.

Publication Title

FUS-CREB3L2/L1-positive sarcomas show a specific gene expression profile with upregulation of CD24 and FOXL1.

Alternate Accession IDs

E-GEOD-24369

Sample Metadata Fields

Specimen part, Disease

View Samples
accession-icon GSE61093
Loss of the tumor suppressor gene AIP mediates the browning of human brown fat tumors
  • organism-icon Homo sapiens
  • sample-icon 85 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

Human brown fat tumors (hibernomas) display concomitant loss of the tumor suppressor genes MEN1 and AIP. In the present study, we hypothesized that the brown fat phenotype is attributed to these mutations. Accordingly, we demonstrate that silencing of AIP in human brown preadipocytic and white fat cell lines results in the induction of the brown fat marker UCP1. In human adipocytic tumors, loss of MEN1 was found both in white (one out of 51 lipomas) and brown fat tumors. In contrast, concurrent loss of AIP was always accompanied by a brown fat morphology. We conclude that this white-to-brown phenotype switch in brown fat tumors is mediated by the loss of AIP.

Publication Title

Loss of the tumour suppressor gene AIP mediates the browning of human brown fat tumours.

Alternate Accession IDs

E-GEOD-61093

Sample Metadata Fields

Specimen part

View Samples
accession-icon GSE54316
Expression data of human fetal liver hematopoietic stem and progenitors cells
  • organism-icon Homo sapiens
  • sample-icon 8 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

GPI-80 defines self-renewal ability in hematopoietic stem cells during human development.

Alternate Accession IDs

E-GEOD-54316

Sample Metadata Fields

Specimen part

View Samples
accession-icon GSE45136
Identification of the chemokine CCL28 as a growth and survival factor for human hematopoietic stem- and progenitor cells
  • organism-icon Homo sapiens
  • sample-icon 9 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

To discover novel growth factors for hematopoietic stem- and progenitor cells (HSPCs), we have assessed cytokine responses of cord blood (CB)-derived CD34+ cells in a high-content growth factor screen. We identify the immunoregulatory chemokine (C-C motif) ligand 28 (CCL28) as a novel growth factor that directly stimulates proliferation of primitive hematopoietic cells from different ontogenetic origins.

Publication Title

Identification of the chemokine CCL28 as a growth and survival factor for human hematopoietic stem and progenitor cells.

Alternate Accession IDs

E-GEOD-45136

Sample Metadata Fields

Specimen part

View Samples
accession-icon GSE54314
Expression data of human fetal liver hematopoietic stem and progenitors cells [Set 1]
  • organism-icon Homo sapiens
  • sample-icon 2 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Advances in pluripotent stem cell and reprogramming technologies have given hope of generating hematopoietic stem cells (HSC) in culture. To succeed, greater understanding of the self-renewing HSC during human development is required. We discovered that glycophosphatidylinositol-anchored surface protein GPI-80 (Vanin 2) defines a distinct subpopulation of human fetal hematopoietic stem/progenitor cells (HSPC) with self-renewal ability. CD34+CD90+CD38-GPI-80+ HSPC were the sole population that maintained proliferative potential and undifferentiated state in bone marrow stroma co-culture, and engrafted in immunodeficient mice. GPI-80 expression also enabled tracking of HSC migration between human fetal hematopoietic niches. The most highly enriched surface protein in GPI-80+ HSPC as compared to their progeny was Integrin alpha-M (ITGAM), which in leukocytes cooperates with GPI-80 to support migration. Knockdown of either GPI-80 or ITGAM was sufficient to perturb undifferentiated HSPC in stroma co-culture. These findings indicate that human fetal HSC utilize common mechanisms with leukocytes for cell-cell interactions governing HSC self-renewal.

Publication Title

GPI-80 defines self-renewal ability in hematopoietic stem cells during human development.

Alternate Accession IDs

E-GEOD-54314

Sample Metadata Fields

Specimen part

View Samples
accession-icon GSE54315
Expression data of human fetal liver hematopoietic stem and progenitors cells [Set 2]
  • organism-icon Homo sapiens
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Advances in pluripotent stem cell and reprogramming technologies have given hope of generating hematopoietic stem cells (HSC) in culture. To succeed, greater understanding of the self-renewing HSC during human development is required. We discovered that glycophosphatidylinositol-anchored surface protein GPI-80 (Vanin 2) defines a distinct subpopulation of human fetal hematopoietic stem/progenitor cells (HSPC) with self-renewal ability. CD34+CD90+CD38-GPI-80+ HSPC were the sole population that maintained proliferative potential and undifferentiated state in bone marrow stroma co-culture, and engrafted in immunodeficient mice. GPI-80 expression also enabled tracking of HSC migration between human fetal hematopoietic niches. The most highly enriched surface protein in GPI-80+ HSPC as compared to their progeny was Integrin alpha-M (ITGAM), which in leukocytes cooperates with GPI-80 to support migration. Knockdown of either GPI-80 or ITGAM was sufficient to perturb undifferentiated HSPC in stroma co-culture. These findings indicate that human fetal HSC utilize common mechanisms with leukocytes for cell-cell interactions governing HSC self-renewal.

Publication Title

GPI-80 defines self-renewal ability in hematopoietic stem cells during human development.

Alternate Accession IDs

E-GEOD-54315

Sample Metadata Fields

Specimen part

View Samples
accession-icon SRP091781
Identification of glucocorticoid-dependent circadian genes in the cochlea
  • organism-icon Mus musculus
  • sample-icon 33 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

The cochlea possesses a robust circadian clock machinery that regulates auditory function. How the cochlear clock is influenced by the circadian system remains unknown. Here we show that cochlear rhythms are system-driven and require local Bmal1 as well as central input from the suprachiasmatic nuclei (SCN). SCN ablations disrupted the circadian expression of the core clock genes in the cochlea. Since the circadian secretion of glucocorticoids (GCs) is controlled by the SCN and that GCs are known to modulate auditory function, we assessed their influence on circadian gene expression. Removal of circulating GCs by adrenalectomy (ADX) did not have a major impact on core clock gene expression in the cochlea. Rather it abolished the transcription of clock-controlled genes involved in inflammation. ADX abolished the known differential auditory sensitivity to day and night noise trauma and prevented the induction of GABA-ergic and glutamate receptors mRNA transcripts. However, these improvements were unrelated to changes at the synaptic level suggesting other cochlear functions may be involved. Due to this circadian regulation of noise sensitivity by GCs, we evaluated the actions of the synthetic glucocorticoid dexamethasone (DEX) at different times of the day. DEX was effective in protecting from acute noise trauma only when administered during daytime, when circulating glucocorticoids are low, indicating that chronopharmacological approaches are important for obtaining optimal treatment strategies for hearing loss. GCs appear as a major regulator of the differential sensitivity to day or night noise trauma, a mechanism likely involving the circadian control of inflammatory responses. Overall design: Cochlear samples from sham operated or adrenalectomized (ADX) CBA/Sca mice were collected every 4th hour during a 24h period and subjected to RNAseq (n=3 per time point, corresponding to a total of 36 samples).

Publication Title

Circadian Regulation of Cochlear Sensitivity to Noise by Circulating Glucocorticoids.

Alternate Accession IDs

GSE88954

Sample Metadata Fields

Age, Specimen part, Cell line, Subject

View Samples
accession-icon GSE34974
Gene expression of cultured human fetal liver hematopoietic stem and progenitor cells (HSPC) and their supportive ex vivo OP9 stromal niche cells
  • organism-icon Mus musculus, Homo sapiens
  • sample-icon 15 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2), Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Expansion on stromal cells preserves the undifferentiated state of human hematopoietic stem cells despite compromised reconstitution ability.

Alternate Accession IDs

E-GEOD-34974

Sample Metadata Fields

Specimen part, Cell line

View Samples
accession-icon GSE34972
Gene expression analysis of human fetal liver hematopoietic stem and progenitor cells (HSPC) in culture
  • organism-icon Homo sapiens
  • sample-icon 11 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

One of the long-standing goals in the field has been to establish a culture system that would allow maintenance of HSC properties ex vivo. In the absence of such system, the ability to model human hematopoiesis in vitro has been limited, and there has been little progress in the expansion of human HSCs for clinical application. To that end, we defined a mesenchyml stem cell co-culture system for expansion of clonally multipotent human HSPCs that are protected from apoptosis and immediate differentiation, and retain the HSPC phenotype. By performing a genome-wide gene expression analysis of purified HSPCs isolated at different stages of co-culture, we asked at the molecular level, to what degree hematopetic stem cell properties can be preserved during culture. This temporal gene expression data from in vivo derived- and ex vivo expanded human HSPCs will serve as a resource to identify novel regulatory pathways that control HSC properties, and to develop clinically applicable protocols for HSC expansion.

Publication Title

Expansion on stromal cells preserves the undifferentiated state of human hematopoietic stem cells despite compromised reconstitution ability.

Alternate Accession IDs

E-GEOD-34972

Sample Metadata Fields

Specimen part

View Samples
accession-icon GSE23909
Effect of Valproic Acid on Endothelial Cells
  • organism-icon Homo sapiens
  • sample-icon 10 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

Valproic acid (VPA) is a short-chain fatty acid used in the treatment of epilepsy and also considered to be an epigenetic modifier by functioning as a histone deacetylase (HDAC)-inhibitor. The aim of this study was to search for gene altered by VPA in human endothelial cells.

Publication Title

Role of histone acetylation in the stimulatory effect of valproic acid on vascular endothelial tissue-type plasminogen activator expression.

Alternate Accession IDs

E-GEOD-23909

Sample Metadata Fields

Specimen part, Treatment

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
Version 1.42.67-hotfix - .0.0