refine.bio
  • Search
      • Normalized Compendia
      • RNA-seq Sample Compendia
  • Docs
  • About
  • My Dataset
github link
Showing
of 837 results
Sort by

Filters

Technology

Platform

accession-icon GSE14643
Gene expression following myocardial infarction with and without stem cell transplantation
  • organism-icon Sus scrofa
  • sample-icon 13 Downloadable Samples
  • Technology Badge Icon Affymetrix Porcine Genome Array (porcine)

Description

Background: Bone marrow-derived multipotent progenitor cell (MPC) transplantation leads to short term functional and bioenergetic improvement in a porcine model of postinfarction Left Ventricular (LV) remodeling despite a low engraftment rate. However, the long term outcome after MPC transplantation is unknown.

Publication Title

Long-term functional improvement and gene expression changes after bone marrow-derived multipotent progenitor cell transplantation in myocardial infarction.

Sample Metadata Fields

Sex, Specimen part, Treatment

View Samples
accession-icon GSE2852
Ochratoxin A study on rat liver and kidney gene expression
  • organism-icon Rattus norvegicus
  • sample-icon 60 Downloadable Samples
  • Technology Badge Icon Affymetrix Rat Genome U34 Array (rgu34a), Affymetrix Murine Genome U74A Version 2 Array (mgu74av2)

Description

Ochratoxin A gene expression profiling in liver and kidney, with time points of exposure from 7 days to 12 motnhs

Publication Title

A toxicogenomics approach to identify new plausible epigenetic mechanisms of ochratoxin a carcinogenicity in rat.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon GSE8646
The Hay Wells Syndrome-Derived TAp63alphaQ540L Mutant Has Impaired Transcriptional and Cell Growth Regulatory Activity
  • organism-icon Homo sapiens
  • sample-icon 11 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

p63 mutations have been associated with several human hereditary disorders characterized by ectodermal dysplasia such as EEC syndrome, ADULT syndrome and AEC syndrome . The location and functional effects of the mutations that underlie these syndromes reveal a striking genotype-phenotype correlation. Unlike EEC and ADULT that result from missense mutations in the DNA-binding domain of p63, AEC is solely caused by missense mutations in the SAM domain of p63. We report a study on the TAp63a isoform, the first to be expressed during development of the embryonic epithelia, and on its naturally occurring Q540L mutant derived from an AEC patient. To assess the effects of the Q540L mutation, we generated stable cell lines expressing TAp63a wt, DeltaNp63 alpha or the TAp63 alpha-Q540L mutant protein and used them to systematically compare the cell growth regulatory activity of the mutant and wt p63 proteins and to generate, by microarray analysis, a comprehensive profile of differential gene expression. We found that the Q540L substitution impairs the transcriptional activity of TAp63a and causes misregulation of genes involved in the control of cell growth and epidermal differentiation.

Publication Title

The Hay Wells syndrome-derived TAp63alphaQ540L mutant has impaired transcriptional and cell growth regulatory activity.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon GSE41930
Genome-wide analysis of gene expression in response to bortezomib treatment
  • organism-icon Mus musculus, Homo sapiens
  • sample-icon 44 Downloadable Samples
  • Technology Badge IconIllumina MouseWG-6 v2.0 expression beadchip

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Profiling bortezomib resistance identifies secondary therapies in a mouse myeloma model.

Sample Metadata Fields

Specimen part, Cell line, Time

View Samples
accession-icon GSE41927
Genome-wide analysis of gene expression in response to bortezomib treatment [mouse cell lines I]
  • organism-icon Mus musculus
  • sample-icon 24 Downloadable Samples
  • Technology Badge IconIllumina MouseWG-6 v2.0 expression beadchip

Description

Genome-wide analysis of gene expression in response to bortezomib treatment (33 nM) in cell lines before and after selection for resistance.

Publication Title

Profiling bortezomib resistance identifies secondary therapies in a mouse myeloma model.

Sample Metadata Fields

Specimen part, Cell line, Time

View Samples
accession-icon GSE41928
Genome-wide analysis of gene expression in response to bortezomib treatment [mouse cell lines II]
  • organism-icon Mus musculus
  • sample-icon 20 Downloadable Samples
  • Technology Badge IconIllumina MouseWG-6 v2.0 expression beadchip

Description

Genome-wide analysis of gene expression in response to bortezomib treatment(33 nM) in cell lines before and after selection for resistance.

Publication Title

Profiling bortezomib resistance identifies secondary therapies in a mouse myeloma model.

Sample Metadata Fields

Specimen part, Cell line, Time

View Samples
accession-icon SRP151576
Differential RNA-seq analysis of control vs. dnFGFR2b-expressing mouse otocysts reveals targets of FGFR2b signaling at the beginning of inner ear morphogenesis
  • organism-icon Mus musculus
  • sample-icon 24 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

Induction of dnFGFR2bfor 3 partially overlapping intervals at the early stages of otocyst morphogenesis revealed expected and novel up and downregulated genes that were validated by in situ hybridization analysis. Cell cyle genes were enriched in the downregulated datasets and human hearingloss genes were enriched in the upregulated datasets. Overall design: Differential mRNA expression analysis of pooled Rosa26rtTA/+ (control) and pooled Rosa26rtTA/+;Tg(tetO-s(dn)Fgfr2b)/+ (experimental) embryos induced with doxycycline for the indicated intervals. N=4 biological replicates per treatment (i.e. 4 pregnant females)

Publication Title

Spatial and temporal inhibition of FGFR2b ligands reveals continuous requirements and novel targets in mouse inner ear morphogenesis.

Sample Metadata Fields

Subject

View Samples
accession-icon GSE72039
Defining the microglia response during the time course of chronic neurodegeneration
  • organism-icon Mus musculus
  • sample-icon 16 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.1 ST Array (mogene11st)

Description

In order to study the microglia contribution in neurodegeneration more specifically we established a mouse model of prion disease in which the 79A murine prion strain was introduced by an intraperitoneal route into BALB/cJFms-EGFP/- mice, which express Enhanced Green Fluorescent Protein (EGFP) under control of the C-fms operon. Samples were taken at time points during disease progression and histological analysis of the brain and transcriptional analysis of isolated microglia was carried out. The analysis of isolated microglia revealed a disease specific, highly pro-inflammatory signature in addition to an up-regulation of genes associated with metabolism, respiratory stress and DNA repair. This study strongly supports the growing recognition of the importance of microglia within the prion disease process and identifies the nature of the response through gene expression analysis of isolated microglia.

Publication Title

Defining the Microglia Response during the Time Course of Chronic Neurodegeneration.

Sample Metadata Fields

Sex, Specimen part

View Samples
accession-icon GSE12956
Arx acts as a key selector gene of the ventral telencephalon mainly through its repression transcriptional activity
  • organism-icon Mus musculus
  • sample-icon 10 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

The homeobox containing gene Arx is expressed during ventral telencephalon development and it is required for correct GABAergic interneuron tangential migration from the ganglionic eminences to the olfactory bulbs, cerebral cortex and striatum. Its human ortholog is associated with a variety of neurological clinical manifestations whose syntoms are compatible with a loss of cortical interneurons and altered basal ganglia related-activities in humans. Herein, we reported the identification by global expression profiling of a group of genes whose expression is consistently altered in Arx mutant ganglionic eminences. Following analysis revealed the striking ectopic expression in the ganglionic eminences of a number of genes normally not, or only marginally, expressed in the ventral telencephalon. Among them, we functionally analyzed Ebf3, whose ectopic expression in ventral telencephalon is preventingneuronal tangential migration. Further, we showed that Arx is sufficient to repress Ebf3 endogenous expression and that its silencing in Arx mutant tissue might marginally rescue tangential cell movements. Together, these data provide an initial analysis of the molecular pathways regulated by Arx and how their networking might regulate those specific cellular processes during telencephalon development strongly altered by loss of Arx.

Publication Title

Arx acts as a regional key selector gene in the ventral telencephalon mainly through its transcriptional repression activity.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon GSE74079
Expression data from GSS/101LL brain regions
  • organism-icon Mus musculus
  • sample-icon 23 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 2.1 ST Array (mogene21st)

Description

Gerstmann Strausller Scheinker (GSS) human prion disease homogenate is i.c. inoculated into mice exhibiting a proline to leucine alteration at codon 101 of the murine prion protein gene (101LL). This results in a disease with an incubation period of approximately 291 days. Normal brain homogenate i.c. inoculated into 101LL mice which are aged matched are used as controls.

Publication Title

Distribution of Misfolded Prion Protein Seeding Activity Alone Does Not Predict Regions of Neurodegeneration.

Sample Metadata Fields

Sex, 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