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accession-icon GSE65464
Changes in global gene expression in SIN1 knock-out murine epithelial fibroblasts
  • organism-icon Mus musculus
  • sample-icon 3 Downloadable Samples
  • Technology Badge Icon

Description

RNA from wt and SIN1 knock-out MEF cell lines were compared

Publication Title

mTORC2 Responds to Glutamine Catabolite Levels to Modulate the Hexosamine Biosynthesis Enzyme GFAT1.

Sample Metadata Fields

Specimen part

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accession-icon GSE5338
In vivo function of NR2E3 in establishing photoreceptor identity during mammalian retinal development
  • organism-icon Mus musculus
  • sample-icon 8 Downloadable Samples
  • Technology Badge Icon

Description

Rod and cone photoreceptors in mammalian retina are generated from common pool(s) of neuroepithelial progenitors. NRL, CRX and NR2E3 are key transcriptional regulators that control photoreceptor differentiation. Mutations in NR2E3, a rod-specific orphan nuclear receptor, lead to loss of rods, increased density of S-cones, and supernormal S-cone-mediated vision in humans. To better understand its in vivo function, NR2E3 was expressed ectopically in the Nrl-/- retina, where post-mitotic precursors fated to be rods develop into functional S-cones similar to the human NR2E3 disease. Expression of NR2E3 in the Nrl-/- retina completely suppressed cone differentiation and resulted in morphologically rod-like photoreceptors, which were not functional. Gene profiling of FACS-purified photoreceptors confirmed the role of NR2E3 as a strong suppressor of cone genes and an activator of a subset of rod genes (including rhodopsin) in vivo. Ectopic expression of NR2E3 in cone precursors and differentiating S-cones of wild type retina also generates rod-like cells. The dual regulatory function of NR2E3 is not dependent upon the presence of NRL and/or CRX, but on the timing and level of its expression. Our studies reveal a critical role of NR2E3 in establishing functional specificity of post-mitotic photoreceptor precursors during retinal neurogenesis.

Publication Title

In vivo function of the orphan nuclear receptor NR2E3 in establishing photoreceptor identity during mammalian retinal development.

Sample Metadata Fields

Sex, Specimen part

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accession-icon GSE45121
Expression data from miR-203 induction in mouse skin
  • organism-icon Mus musculus
  • sample-icon 4 Downloadable Samples
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Description

We identify numerous miR-203 in vivo targets that are highly enriched for the promotion of cell cycle and cell division. Importantly, individual targets including p63, Skp2 and Msi2 play distinct roles downstream of miR-203 to regulate the cell cycle and long-term proliferation. Together, our findings reveal rapid and widespread impact of miR-203 on the self-renewal program during the epidermal differentiation and provide mechanistic insights for the potent role of miR-203 where coordinated repression of multiple targets is required for the function of this miRNA.

Publication Title

Rapid and widespread suppression of self-renewal by microRNA-203 during epidermal differentiation.

Sample Metadata Fields

Specimen part

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accession-icon GSE13196
Expression data from zebrafish pineal gland
  • organism-icon Danio rerio
  • sample-icon 3 Downloadable Samples
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Description

Microarray data allowed detection of genes that are highly expressed in the pineal gland.

Publication Title

A new cis-acting regulatory element driving gene expression in the zebrafish pineal gland.

Sample Metadata Fields

Sex

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accession-icon GSE9630
Expression data from mouse liver
  • organism-icon Mus musculus
  • sample-icon 58 Downloadable Samples
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Description

Exposure to high levels of arsenic in drinking water is associated with several types of cancers including lung, bladder and skin, as well as vascular disease and diabetes. Drinking water standards are based primarily on epidemiology and extrapolation from higher dose experiments, rather than measurements of phenotypic changes associated with chronic exposure to levels of arsenic similar to the current standard of 10ppb, and little is known about the difference between arsenic in food as opposed to arsenic in water. Measurement of phenotypic changes at low doses may be confounded by the effect of laboratory diet, in part because of trace amounts of arsenic in standard laboratory chows, but also because of broad metabolic changes in response to the chow itself. Finally, this series contrasts 8hr, 1mg/kg injected arsenic with the various chronic exposures, and also contrasts the acute effects of arsenic, dexamethasone or their combination. Male C57BL/6 mice were fed on two commercially available laboratory diets (LRD-5001 and AIN-76A) were chronically exposed, through drinking water or food, to environmentally relevant concentrations of sodium arsenite, or acutely exposed to dexamethasone.

Publication Title

Laboratory diet profoundly alters gene expression and confounds genomic analysis in mouse liver and lung.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE106788
Identification of SoxC-regulated genes during neurogenesis in the developing spinal cord
  • organism-icon Gallus gallus, Mus musculus
  • sample-icon 4 Downloadable Samples
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Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

The transcription factor prospero homeobox protein 1 is a direct target of SoxC proteins during developmental vertebrate neurogenesis.

Sample Metadata Fields

Specimen part

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accession-icon GSE106786
Identification of SoxC-regulated genes during neurogenesis in the developing spinal cord [mouse]
  • organism-icon Mus musculus
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon

Description

The HMG-domain containing SoxC transcription factors Sox4 and Sox11 are expressed in the vertebrate central nervous system in neuronal precursors and neuroblasts. They are required during early stages of neurogenesis.

Publication Title

The transcription factor prospero homeobox protein 1 is a direct target of SoxC proteins during developmental vertebrate neurogenesis.

Sample Metadata Fields

Specimen part

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accession-icon GSE26001
Microarray gene expression data from Hdh knock-out, wild-type and knock-in embryonic stem cells
  • organism-icon Mus musculus
  • sample-icon 24 Downloadable Samples
  • Technology Badge Icon

Description

Huntington's disease (HD) features a unique disease-initiating mechanism hypothesized to entail an impact of the CAG repeat encoded polyglutamine region on the full-length huntingtin protein, with dominant effects that are continuous with CAG size, in a simple gain of function. To evaluate these predictions, we generated a series of heterozygous Hdh CAG knock-in mouse embryonic stem (ES) cell lines, with 18, 48, 89, 109 CAGs, and found that a continuous analytic strategy efficiently identified, from genome-wide datasets, 73 genes and 172 pathways whose expression varied continuously with CAG length. The CAG-correlated genes were distinct from the set of 754 genes that distinguished huntingtin null ES cells from wild-type controls, and CAG-correlated pathways did not display a one-to-one correspondence with the 238 pathways altered in huntingtin null ES cells. Rather, the genes that varied with CAG size were either members of the same pathways as altered genes in huntingtin null cells or were members of unique pathways related to these pathways. These findings falsified a gain of function/loss of function proposal but were consistent with the simple gain of novel function mechanism hypothesis. The dominant CAG correlated gene expression changes conformed to the genetic features of the HD initiating mechanism and were system-wide and inter-related with pathways perturbed by lack of full-length huntingtin function, urging system-wide approaches for the discovery and validation of potential modulating factors, in the search for effective HD therapeutics.

Publication Title

HD CAG-correlated gene expression changes support a simple dominant gain of function.

Sample Metadata Fields

Cell line

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accession-icon GSE27038
Expression data from the Ire1 null and control murine livers in the absence or presence of ER stress
  • organism-icon Mus musculus
  • sample-icon 12 Downloadable Samples
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Description

Ire1 conditional null or control mice of 3-months old were injected intraperitoneally with TM or vehicle.

Publication Title

The unfolded protein response transducer IRE1α prevents ER stress-induced hepatic steatosis.

Sample Metadata Fields

Specimen part

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accession-icon GSE59930
Peroxisomes and mitochondria are dysfunctional in obese diabetic (db/db) mice with fatty liver
  • organism-icon Mus musculus
  • sample-icon 8 Downloadable Samples
  • Technology Badge Icon

Description

Major causes of lipid accumulation in liver are increased import, synthesis or decreased catabolism of fatty acids. The latter is caused by dysfunction of cellular organelle controlling energy homeostasis, i.e. mitochondria. However, peroxisomes appear to be an important organelle in lipid metabolism of hepatocytes, but little is known about their role in the development of non-alcoholic fatty liver disease (NAFLD). To investigate the role of peroxisomes next to mitochondria in excessive hepatic lipid accumulation we used the leptin resistant db/db mice on C57BLKS background, a mouse model that develops hyperphagia induced diabetes with obesity and NAFLD.

Publication Title

Peroxisomes compensate hepatic lipid overflow in mice with fatty liver.

Sample Metadata Fields

Sex, Age, Specimen part

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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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