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accession-icon GSE46017
Transcriptional response to Smarcb1 re-expression in murine derived Smarcb1 deficient p53 null tumors
  • organism-icon Mus musculus
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

SMARCB1 (Snf5/Ini1/Baf47) is a potent tumor suppressor, the loss of which serves as the diagnostic feature in Malignant Rhabdoid Tumors (MRT) and Atypical Teratoid/Rhabdoid Tumors (AT/RT), two highly aggressive forms of pediatric neoplasms. Here, we restore Smarcb1 expression in cells derived from Smarcb1-deficient tumors which developed in Smarcb1-heterozygous p53-/- mice.

Publication Title

Loss of IGFBP7 expression and persistent AKT activation contribute to SMARCB1/Snf5-mediated tumorigenesis.

Sample Metadata Fields

Specimen part, Cell line

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accession-icon GSE11342
Gene expression of Peg-interferon alfa-2b plus ribavirin in hepatitis C patients during the first 10 weeks of treatment
  • organism-icon Homo sapiens
  • sample-icon 152 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A Array (hgu133a)

Description

Study of PBMC gene expression during the first 10 weeks of therapy with Pegylated-interferon-alfa2b (PegIntronTM) and ribavirin (administered by weight) in HCV patients.

Publication Title

Cyclic changes in gene expression induced by Peg-interferon alfa-2b plus ribavirin in peripheral blood monocytes (PBMC) of hepatitis C patients during the first 10 weeks of treatment.

Sample Metadata Fields

Subject

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accession-icon GSE1614
Caco-2 differentiation
  • organism-icon Homo sapiens
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U95 Version 2 Array (hgu95av2)

Description

This is an analysis of Caco-2 BBe cell spontaneous differentiation. JF2dR1-JF2dR4 = proliferating cells; JF8dR1-JF8dR4 = 4 d post-confluent; JF15dR1-JF15dR4 = 11 d pc, differentiated

Publication Title

Gene expression profiling of Caco-2 BBe cells suggests a role for specific signaling pathways during intestinal differentiation.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE15407
The Nucleus Accumbens Shell and Central Nucleus of the Amygdala of Alcohol-Preferring Rats Following Binge-Drinking
  • organism-icon Rattus norvegicus
  • sample-icon 96 Downloadable Samples
  • Technology Badge Icon Affymetrix Rat Genome 230 2.0 Array (rat2302)

Description

The objective of this study was to determine changes in gene expression within the extended amygdala following binge-like drinking by alcohol-preferring (P) rats. Adult male P rats were given 1-hr access to 15 and 30% ethanol (EtOH) three times daily for 8 weeks. Rats (n = 10/time point for EtOH and n = 6/time point for water) were killed by decapitation 1, 6 and 24 hr after the last drinking episode. Brains were extracted and rapidly frozen in isopentane in dry ice. RNA was prepared from individual micropunch samples of the nucleus accumbens shell (ACB-sh) and central nucleus of the amygada (CeA); microarray analyses were conducted with Affymetrix Rat 230.2 chips. EtOH intakes were 1.5-2 g/kg/session. Because too few genes changed at the individual time points, an overall effect, comparing the water and EtOH groups, was determined. In the ACB-sh and CeA, there were 276 and 402 probe sets for named genes, respectively, that were different between the two groups. There were 1.5- to 3.5- fold more genes up-regulated than down-regulated in both regions, with most differences between 1.1- to 1.2-fold. Although there were several significant Biological Processes categories in common between the 2 regions (e.g., synaptic transmission, neurite development), there were few genes in common between the two regions that differed between the EtOH and water groups. Overall, the results suggest that chronic binge-like alcohol drinking by P rats produces changes in the expression of genes that could alter neuronal function by different mechanisms in the ACB-sh and CeA.

Publication Title

Changes in gene expression in regions of the extended amygdala of alcohol-preferring rats after binge-like alcohol drinking.

Sample Metadata Fields

Specimen part

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accession-icon GSE145574
Embryonic ethanol exposure alters expression of sox2 and other early transcripts in zebrafish, producing gastrulation defects
  • organism-icon Danio rerio
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Zebrafish Genome Array (zebrafish)

Description

Ethanol exposure during prenatal development causes fetal alcohol spectrum disorder (FASD), the most frequent preventable birth defect and neurodevelopmental disability syndrome. The molecular targets of ethanol toxicity during development are poorly understood. Developmental stages surrounding gastrulation are very sensitive to ethanol exposure. To understand the effects of ethanol on early transcripts during embryogenesis, we treated zebrafish embryos with ethanol during pre-gastrulation period and examined the transcripts by Affymetrix GeneChip microarray before gastrulation. We identified 521 significantly dysregulated genes, including 61 transcription factors in ethanol-exposed embryos. Sox2, the key regulator of pluripotency and early development was significantly reduced. Functional annotation analysis showed enrichment in transcription regulation, embryonic axes patterning, and signaling pathways, including Wnt, Notch and retinoic acid. We identified all potential genomic targets of 25 dysregulated transcription factors and compared their interactions with the ethanol-dysregulated genes. This analysis predicted that Sox2 targeted a large number of ethanol-dysregulated genes. A gene regulatory network analysis showed that many of the dysregulated genes are targeted by multiple transcription factors. Injection of sox2 mRNA partially rescued ethanol-induced gene expression, epiboly and gastrulation defects. Additional studies of this ethanol dysregulated network may identify therapeutic targets that coordinately regulate early development.

Publication Title

Embryonic ethanol exposure alters expression of sox2 and other early transcripts in zebrafish, producing gastrulation defects.

Sample Metadata Fields

Treatment

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accession-icon GSE15415
Candidate genes for alcohol preference in alcohol-preferring and non-preferring reciprocal congenic rats
  • organism-icon Rattus norvegicus
  • sample-icon 80 Downloadable Samples
  • Technology Badge Icon Affymetrix Rat Genome 230 2.0 Array (rat2302)

Description

The goal of this study was to identify candidate genes that may influence alcohol consumption by comparing gene expression in 5 brain regions of alcohol-nave iP and P.NP rats.

Publication Title

Candidate genes for alcohol preference identified by expression profiling in alcohol-preferring and -nonpreferring reciprocal congenic rats.

Sample Metadata Fields

Specimen part

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accession-icon GSE5849
Identification of Candidate Genes for Alcohol Preference by Expression Profiling of Congenic Strains
  • organism-icon Rattus norvegicus
  • sample-icon 60 Downloadable Samples
  • Technology Badge Icon Affymetrix Rat Genome 230 2.0 Array (rat2302)

Description

A highly significant quantitative trait locus (QTL) that influenced alcohol preference was identified in the iP/iNP rats on chromosome 4.

Publication Title

Identification of candidate genes for alcohol preference by expression profiling of congenic rat strains.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE4494
Functional Gene Expression Differences between Inbred Alcohol-Preferring (iP) and non-preferring (iNP) Rats
  • organism-icon Rattus norvegicus
  • sample-icon 59 Downloadable Samples
  • Technology Badge Icon Affymetrix Rat Genome U34 Array (rgu34a)

Description

The objective of this study was to test the hypothesis that innate differences in gene expression in the brain could

Publication Title

Functional gene expression differences between inbred alcohol-preferring and -non-preferring rats in five brain regions.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE12066
Segregation of genes influencing skeletal phenotypes in congenic P/NP rats
  • organism-icon Rattus norvegicus
  • sample-icon 20 Downloadable Samples
  • Technology Badge Icon Affymetrix Rat Genome 230 2.0 Array (rat2302)

Description

Bone mineral density and structure candidate gene analysis in alcohol-non-preferring (NP), alcohol-preferring (P), congenic NP (NP.P) and congenic P (P.NP) rats

Publication Title

Identification of genes influencing skeletal phenotypes in congenic P/NP rats.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE65391
Longitudinal transcriptional pediatric SLE study with clinical parameters
  • organism-icon Homo sapiens
  • sample-icon 996 Downloadable Samples
  • Technology Badge IconIllumina HumanHT-12 V4.0 expression beadchip

Description

The goal of the study was to identify transcriptional correlates of SLE disease activity both at the cohort and at the individual levels. To do so, we longitudinally profiled the whole blood transcriptomes of 158 SLE patients by microarray for up to 4 years, yielding 924 SLE samples and 48 matched pediatric healthy samples. The transcriptional data are complemented by demographic, laboratory and clinical data.

Publication Title

Personalized Immunomonitoring Uncovers Molecular Networks that Stratify Lupus Patients.

Sample Metadata Fields

Sex, Age, Specimen part, Disease, Disease stage, Treatment, Race, Subject

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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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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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