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accession-icon GSE18224
Female sex and oestrogen receptor attenuate cardiac remodelling and apoptosis in pressure overload
  • organism-icon Mus musculus
  • sample-icon 31 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Aims: We investigate sex differences and the role of oestrogen receptor beta (ERbeta) in a mouse model of pressure overload-induced myocardial hypertrophy. Methods and results: We performed transverse aortic constriction (TAC) or sham surgery in male and female wild-type (WT) and ERbeta knockout (ERbeta-/-) C57Bl6 mice. All mice were characterised by echocardiography and haemodynamic measurements and were sacrificed nine weeks after surgery. Left ventricular (LV) samples were analysed by microarray profiling, real-time RT-PCR and histology. After nine weeks, WT males showed more hypertrophy and heart failure signs than WT females. Notably, WT females developed a concentric form of hypertrophy, while males developed eccentric hypertrophy. These sex differences were abolished in ERbeta-/- mice. ERbeta deletion augmented the TAC-induced increase in cardiomyocyte diameter in both sexes. Gene expression profiling revealed that male WT hearts had a stronger induction of matrix-related genes and a stronger repression of mitochondrial genes than female hearts. ERbeta-/- mice exhibited a different transcriptome. Induction of pro-apoptotic genes after TAC occurred in ERbeta-/- mice of both sexes with a stronger expression in ERbeta-/- males. Histological analysis revealed, that cardiac fibrosis was more pronounced in male WT TAC than in female mice. This was abolished in ERbeta-/- mice. Apoptosis was significantly induced in both sexes of ERbeta-/- TAC mice, but it was most prominent in males. Conclusion: Female sex offers protection against ventricular chamber dilation in the TAC model. Both the female sex and ERbeta attenuate the development of fibrosis and apoptosis; thus slowing the progression to heart failure.

Publication Title

Female sex and estrogen receptor-beta attenuate cardiac remodeling and apoptosis in pressure overload.

Sample Metadata Fields

Sex, Age, Specimen part

View Samples
accession-icon GSE34229
Expression data of liver samples of dex or vehicle treated wildtype and HDAC6- knockout C57Bl/6 mice respectively
  • organism-icon Mus musculus
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

In the present study, we investigated the importance of histone deacetylase 6 (HDAC6) for glucocorticoid receptor (GR) mediated effects on glucose metabolism, and its potential as a therapeutic target for the prevention of glucocorticoid (GC)-induced diabetes. Dexamethasone (dex)-induced hepatic glucose output and GR translocation were analysed in wildtype (wt) and HDAC6-deficient (HDAC6ko) mice. The effect of the specific HDAC6-inhibitor tubacin was analysed in-vitro. Wt and HDAC6ko mice were subjected to 3 weeks dex treatment before analysis of glucose and insulin tolerance. HDAC6ko mice showed impaired dex-induced hepatic GR translocation. Accordingly, dex induced expression of a large number of hepatic genes was significantly attenuated in mice lacking HDAC6 and by tubacin in-vitro. Glucose output of primary hepatocytes from HDAC6ko mice was diminished. A significant improvement of dex-induced whole-body glucose intolerance as well as insulin resistance in HDAC6ko mice compared to wt littermates was observed. The present study demonstrates that HDAC6 is an essential regulator of hepatic GC stimulated gluconeogenesis and impairment of whole body glucose metabolism through modification of GR nuclear translocation. Selective pharmacological inhibition of HDAC6 may provide a future therapeutic option against the pro-diabetogenic actions of GCs.

Publication Title

Histone deacetylase 6 (HDAC6) is an essential modifier of glucocorticoid-induced hepatic gluconeogenesis.

Sample Metadata Fields

Sex, Specimen part, Treatment

View Samples
accession-icon GSE23844
Analysis of Notch signaling on Xenopus epidermis
  • organism-icon Xenopus laevis
  • sample-icon 5 Downloadable Samples
  • Technology Badge Icon Affymetrix Xenopus laevis Genome Array (xenopuslaevis)

Description

Analysis of epithelial explants injected with the intracellular domain of Notch (ICD) to block the formation of multi-ciliate and proton secreting cells or with dominant negative human Mastermind (HMM) to induce the formation of ectopic multi-ciliate and proton secreting cells. Results show which genes are up or down-regulated when HMM is compared to ICD.

Publication Title

Specification of ion transport cells in the Xenopus larval skin.

Sample Metadata Fields

Specimen part, Treatment

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accession-icon GSE32331
Early downstream targets of Notch signaling which contribute to multiciliate cell fate
  • organism-icon Xenopus laevis
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon Affymetrix Xenopus laevis Genome 2.0 Array (xlaevis2)

Description

Analysis of epithelial explants injected with the intracellular domain of Notch (ICD) to block the formation of multi-ciliate and proton secreting cells or with dominant negative human Mastermind (HMM) or a DNA binding mutant of Mastermind (DBM) to induce the formation of ectopic multi-ciliate and proton secreting cells. Results show which genes are up or down-regulated when DBM/HMM are compared to ICD.

Publication Title

Multicilin promotes centriole assembly and ciliogenesis during multiciliate cell differentiation.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon GSE12613
Effect of FoxJ1 on expression of cilia genes
  • organism-icon Xenopus laevis
  • sample-icon 5 Downloadable Samples
  • Technology Badge Icon Affymetrix Xenopus laevis Genome Array (xenopuslaevis)

Description

Analysis of epithelial explants injected with the intracellular domain of Notch (ICD) to block the formation of multi-ciliate cells, either alone or along with FoxJ1. FoxJ1 misexpression leads to the induction fo ectopic cilia in Xenopus laevis epithelia. Results show which genes are affected by FoxJ1 during the induction of ectopic cilia.

Publication Title

The forkhead protein Foxj1 specifies node-like cilia in Xenopus and zebrafish embryos.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon GSE29515
The transcriptional program controlled by Runx1 during early hematopoietic development
  • organism-icon Mus musculus
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

The transcriptional programme controlled by Runx1 during early embryonic blood development.

Sample Metadata Fields

Specimen part, Cell line

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accession-icon GSE29112
The transcriptional program controlled by Runx1 during early hematopoietic development (expression data)
  • organism-icon Mus musculus
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Transcription factors have long been recognised as powerful regulators of mammalian development, yet it is largely unknown how individual key regulators operate within wider regulatory networks. Here we have used a combination of global gene expression and chromatin-immunoprecipitation approaches across four ES-cell-derived populations of increasing haematopoietic potential to define the transcriptional programme controlled by Runx1, an essential regulator of blood cell specification. Integrated analysis of these complementary genome-wide datasets allowed us to construct a global regulatory network model, which suggested that core regulatory circuits are activated sequentially during blood specification, but will ultimately collaborate to control many haematopoietically expressed genes. Using the CD41/integrin alpha 2b gene as a model, cellular and in vivo studies showed that CD41 is controlled by both early and late circuits in fully specified blood cells, but initiation of CD41 expression critically depends on a later subcircuit driven by Runx1. Taken together, this study represents the first global analysis of the transcriptional programme controlled by any key haematopoietic regulator during the process of early blood cell specification. Moreover, the concept of interplay between sequentially deployed core regulatory circuits is likely to represent a design principle widely applicable to the transcriptional control of mammalian development.

Publication Title

The transcriptional programme controlled by Runx1 during early embryonic blood development.

Sample Metadata Fields

Specimen part, Cell line

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accession-icon GSE62918
Expression data from Escherichia coli strains with increased or decreased levels of Obg (ObgE, CgtA, YhbZ)
  • organism-icon Escherichia coli
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix E. coli Genome 2.0 Array (ecoli2)

Description

We measured transcriptional changes resulting from overexpression or downregulation of the GTPase Obg.

Publication Title

Obg and Membrane Depolarization Are Part of a Microbial Bet-Hedging Strategy that Leads to Antibiotic Tolerance.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon GSE34006
Role of Adenosine 2A Receptors (A2AR) on regulatory T cells (Tregs)
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

The adenosine 2A receptor (A2AR) is expressed on regulatory T cells (Tregs), but the functional significance is currently unknown. We compared the gene expression between wild-type (WT) and A2AR knockout (KO) Tregs and between WT Tregs treated with vehicle or a selective A2AR agonist.

Publication Title

Autocrine adenosine signaling promotes regulatory T cell-mediated renal protection.

Sample Metadata Fields

Specimen part

View Samples
accession-icon GSE41386
Role of REST in the pathogenesis of uterine fibroids
  • organism-icon Homo sapiens
  • sample-icon 9 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

The loss of REST in uterine fibroids promotes aberrant gene expression and enables mTOR pathway activation

Publication Title

Loss of the repressor REST in uterine fibroids promotes aberrant G protein-coupled receptor 10 expression and activates mammalian target of rapamycin pathway.

Sample Metadata Fields

Specimen part, Treatment

View Samples
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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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