refine.bio
  • Search
      • Normalized Compendia
      • RNA-seq Sample Compendia
  • Docs
  • About
  • My Dataset
github link
Showing
of 1395 results
Sort by

Filters

Technology

Platform

accession-icon GSE28706
CO1 and CO2 network analysis in poplar
  • organism-icon Populus tremula x populus alba
  • sample-icon 16 Downloadable Samples
  • Technology Badge Icon Affymetrix Poplar Genome Array (poplar)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Overexpression of CONSTANS homologs CO1 and CO2 fails to alter normal reproductive onset and fall bud set in woody perennial poplar.

Sample Metadata Fields

Specimen part

View Samples
accession-icon GSE28693
CO2 network analysis in poplar
  • organism-icon Populus tremula x populus alba
  • sample-icon 8 Downloadable Samples
  • Technology Badge Icon Affymetrix Poplar Genome Array (poplar)

Description

We conducted microarray experiments by comparing constitutive constructs with appropriate controls, followed by the identification of downstream targets of Pro35S:CO2.

Publication Title

Overexpression of CONSTANS homologs CO1 and CO2 fails to alter normal reproductive onset and fall bud set in woody perennial poplar.

Sample Metadata Fields

Specimen part

View Samples
accession-icon GSE28689
CO1 network analysis in poplar
  • organism-icon Populus tremula x populus alba
  • sample-icon 8 Downloadable Samples
  • Technology Badge Icon Affymetrix Poplar Genome Array (poplar)

Description

We conducted microarray experiments by comparing constitutive constructs with appropriate controls, followed by the identification of downstream targets of Pro35S:CO1

Publication Title

Overexpression of CONSTANS homologs CO1 and CO2 fails to alter normal reproductive onset and fall bud set in woody perennial poplar.

Sample Metadata Fields

Specimen part

View Samples
accession-icon GSE32885
Loss of heat shock protein HSPA4 aggravates pressure overload-induced myocardial damage
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

Failure of molecular chaperones to direct the correct folding of newly synthesized proteins leads to the accumulation of misfolded proteins in cells. HSPA4 is a member of the heat shock protein 110 family (HSP110) that acts as a nucleotide exchange factor of HSP70 chaperones. We found that the expression of HSPA4 is upregulated in murine hearts subjected to pressure overload and in failing human hearts. To investigate the cardiac function of HSPA4, Hspa4 knockout (KO) mice were generated and exhibited cardiac hypertrophy and fibrosis. Hspa4 KO hearts were characterized by a significant increase in heart weight/body weight ratio, elevated expression of hypertrophic and fibrotic gene markers, and concentric hypertrophy with preserved contractile functions. Cardiac hypertrophy in Hspa4 KO hearts was associated with enhanced activation of gp130-STAT3, CaMKII, and calcineurin-NFAT signaling. Further analyses revealed a significant increase in cross sectional area of cardiomyocytes, and in expression levels of hypertrophic markers in cultured neonatal Hspa4 KO cardiomyocytes suggesting that the hypertrophy of mutant mice was a result of primary defects in cardiomyocytes. Gene expression profile in hearts of 3.5-week-old mice revealed a differentially expressed gene sets related to ion channels and stress response. Taken together, these results reveal that HSPA4 is implicated in protection against pressure overload-induced heart failure.

Publication Title

Targeted disruption of Hspa4 gene leads to cardiac hypertrophy and fibrosis.

Sample Metadata Fields

Sex

View Samples
accession-icon GSE74120
Gene profile analysis of sorted Sca1+/cKit- BMCs obtained from young and aged mice bearing tumor or not
  • organism-icon Mus musculus
  • sample-icon 14 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 2.0 ST Array (mogene20st)

Description

Sca1+/cKit hematopoietic BMCs of hosts bearing primary tumors promote the growth of distant tumors that form with a myofibroblast-rich, desmoplastic stroma. BMCs from old mice bearing primary tumors lack this ability

Publication Title

Hematopoietic Age at Onset of Triple-Negative Breast Cancer Dictates Disease Aggressiveness and Progression.

Sample Metadata Fields

Sex, Specimen part

View Samples
accession-icon GSE75333
Aging reduces the pro-tumorigenic potential of bone marrow cells and influences triple-negative breast cancer progression
  • organism-icon Homo sapiens
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

To examine the effects of recombinant granulin on human mammary stromal fibroblasts, we cultured immortalized GFP+ normal human mammary fibroblasts in the presence of recombinant human granulin (1ug/ml) or PBS every 24h for 6 days. To generate GRN-independent CAFs, we injected immortalized GFP+ human mammary fibroblasts, MCF7Ras human breast carcinoma cells, and 20% Matrigel subcutaneously into nude mice. Tumors were allowed to form for a period of 45 days. GFP+ fibroblasts were isolated from tumors by mincing the tumors, dissociating, and culturing in the presence of 1 ug/ml puromycin for ~3-4 weeks. CAF purity was confirmed by ensuring that 100% of the population was GFP-positive.

Publication Title

Hematopoietic Age at Onset of Triple-Negative Breast Cancer Dictates Disease Aggressiveness and Progression.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon GSE15119
Mammary tumors in transgenic mice expressing constitutively active and C-terminally truncated variants of STAT5
  • organism-icon Mus musculus
  • sample-icon 16 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430A 2.0 Array (mouse430a2)

Description

Stat5 is a latent transcription factor that regulates essential growth and survival functions in normal cells. Constitutive activity of Stat5 and the involvement of its C-terminally truncated variant have been implicated in blood cell malignancies and mammary or breast cancer.

Publication Title

Forced activation of Stat5 subjects mammary epithelial cells to DNA damage and preferential induction of the cellular response mechanism during proliferation.

Sample Metadata Fields

Specimen part, Disease, Disease stage

View Samples
accession-icon SRP045763
Dynamics of gene silencing during X inactivation using allele-specific RNA-Seq
  • organism-icon Mus musculus
  • sample-icon 22 Downloadable Samples
  • Technology Badge Icon

Description

Background: During early embryonic development, one of the two X chromosomes in mammalian female cells is inactivated to compensate for a potential imbalance in transcript levels with male cells containing a single X chromosome. We use mouse female Embryonic Stem Cells (ESCs) with nonrandom XCI and polymorphic X chromosomes to study the dynamics of gene silencing over the inactive X chromosome (Xi) by high-resolution allele-specific RNA-Seq. Results: Induction of XCI by differentiation of female ESCs shows that genes proximal to the X-inactivation center (XIC) are silenced earlier than distal genes, while lowly expressed genes show faster XCI dynamics than highly expressed genes. The active X chromosome shows a minor but significant increase in gene activity during differentiation, resulting in complete dosage compensation in differentiated cell types. Genes escaping XCI show little or no silencing during early propagation of XCI. Using allele-specific RNA-Seq of Neural Progenitor Cells (NPCs) generated from the female ESCs, we identify three regions distal to the XIC that stably escape XCI during differentiation of the female ESCs, as well as during propagation of the NPCs. These regions coincide with Topologically Associated Domains (TADs) as determined in the undifferentiated female ESCs. Also the previously characterized human gene clusters escaping XCI correlate with TADs. Conclusions: Together, the dynamics of gene silencing observed over the Xi during XCI provide further insight in the formation and maintenance of the repressive Xi complex. The association of regions of escape with TADs, in mouse and human, suggests a regulatory role for TADs during propagation of XCI. Overall design: 19 RNA-Seq profiles of mouse ESCs, EpiSCs and NPCs, mostly from distant crosses to allow allele specific mapping. 1 HiC profile of an undifferentiated mouse female ESC line containing a Tsix mutation. Mainly focusing on X inactivation.

Publication Title

Dynamics of gene silencing during X inactivation using allele-specific RNA-seq.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon GSE24609
FT1 and FT2 network analysis in poplar
  • organism-icon Populus tremula x populus tremuloides, Populus tremula x populus alba
  • sample-icon 14 Downloadable Samples
  • Technology Badge Icon Affymetrix Poplar Genome Array (poplar)

Description

We conducted microarray experiments by comparing constitutive and inducible Flowering Locus T1 (FT1) and FT2 constructs with appropriate controls, followed by the identification of common targets of Pro35S:FT1 and ProHSP:FT1 or Pro35S:FT2 and ProHSP:FT2.

Publication Title

FLOWERING LOCUS T duplication coordinates reproductive and vegetative growth in perennial poplar.

Sample Metadata Fields

Specimen part, Treatment

View Samples
accession-icon GSE478
Alveoli loss during caloric restriction time course
  • organism-icon Mus musculus
  • sample-icon 25 Downloadable Samples
  • Technology Badge Icon Affymetrix Murine Genome U74A Version 2 Array (mgu74av2)

Description

Pulmonary alveoli are complex architectural units thought to undergo endogenous or pharmacologically induced programs of regeneration and degeneration. To study the molecular mechanism of alveoli loss mice were calorie restricted at different timepoints. Lungs were harvested and processed for RNA extraction.

Publication Title

Calorie-related rapid onset of alveolar loss, regeneration, and changes in mouse lung gene expression.

Sample Metadata Fields

Time

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