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accession-icon GSE34060
Expression data of Sox9+ and Ngn3+ mouse pancreas cells at different stages of development
  • organism-icon Mus musculus
  • sample-icon 15 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

Genes specific to Sox9+ pancreatic progenitors were identified by comparing the gene expression in embryonic and adult Sox9+ cells.

Publication Title

A Notch-dependent molecular circuitry initiates pancreatic endocrine and ductal cell differentiation.

Sample Metadata Fields

Specimen part

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accession-icon GSE54417
mTORC1 maintains renal tubular homeostasis and is essential in response to ischemic stress
  • organism-icon Mus musculus
  • sample-icon 10 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

The mechanistic target of rapamycin mTORC1 is a key regulator of cell metabolism and autophagy. Despite widespread clinical use of mTOR inhibitors, the role of mTORC1 in renal tubular function and kidney homeostasis remains elusive. By utilizing constitutive and inducible deletion of conditional Raptor alleles in renal tubular epithelial cells, we discovered that mTORC1 deficiency caused a marked concentrating defect, loss of tubular cells and slowly progressive renal fibrosis. Transcriptional profiling revealed that mTORC1 maintains renal tubular homeostasis by controlling mitochondrial metabolism and biogenesis as well as transcellular transport processes involved in counter-current multiplication and urine concentration. Although mTORC2 partially compensated the loss of mTORC1, exposure to ischemia and reperfusion injury exaggerated the tubular damage in mTORC1-deficient mice, and caused pronounced apoptosis, diminished proliferation rates and delayed recovery. These findings identify mTORC1 as an essential regulator of tubular energy metabolism and as a crucial component of ischemic stress responses. Pharmacological inhibition of mTORC1 likely affects tubular homeostasis, and may be particularly deleterious if the kidney is exposed to acute injury. Furthermore, the combined inhibition of mTORC1 and mTORC2 may increase the susceptibility to renal damage.

Publication Title

mTORC1 maintains renal tubular homeostasis and is essential in response to ischemic stress.

Sample Metadata Fields

Specimen part

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accession-icon GSE108904
Heart tissue expression data from dTGR rats treated with or without BAY 41-8543 and Sprague Dawley control rats
  • organism-icon Rattus norvegicus
  • sample-icon 28 Downloadable Samples
  • Technology Badge Icon Affymetrix Rat Gene 2.1 ST Array (ragene21st)

Description

We aimed to characterize the complex cardiovascular effects of NOsGC stimulation using NO-independent stimulator BAY 41-8543 in a double transgenic rat (dTGR) model of HFpEF.

Publication Title

Nitric oxide-sensitive guanylyl cyclase stimulation improves experimental heart failure with preserved ejection fraction.

Sample Metadata Fields

Sex, Specimen part, Treatment

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accession-icon GSE19701
Time series gene expression data from adult rat tail MNs following spinal cord transection
  • organism-icon Rattus norvegicus
  • sample-icon 31 Downloadable Samples
  • Technology Badge Icon Affymetrix Rat Genome 230 2.0 Array (rat2302)

Description

Spinal cord injury leads to impaired motor and sensory functions. After spinal cord injury there is a an initial phase of hypo-reflexia followed by a developing hyper-reflexia, often termed spasticity. Previous studies have suggested a relationship between the reappearence of plateau potentials in motor neurons and the development of spasticity after spinalizaion. To understand the moleclar mechanism behind this pheneomona we examined the transcriptional response of the motor neurons after spinal cord injury as it progress over time.

Publication Title

Transcriptional regulation of gene expression clusters in motor neurons following spinal cord injury.

Sample Metadata Fields

Sex, Specimen part

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accession-icon GSE77112
Regulation of Fetal Liver Growth in a Model of Diet Restriction in the Pregnant Rat
  • organism-icon Rattus norvegicus
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Rat Gene 1.0 ST Array (ragene10st)

Description

The present study was designed to test the hypothesis that limited growth of the fetal liver in the model of maternal fasting is independent of well-characterized signaling mechanisms that are known to regulate somatic growth in adult animals.

Publication Title

Regulation of fetal liver growth in a model of diet restriction in the pregnant rat.

Sample Metadata Fields

Specimen part, Treatment

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accession-icon SRP043962
Nuclear stability and transcriptional directionality separate functionally distinct RNA species
  • organism-icon Homo sapiens
  • sample-icon 9 Downloadable Samples
  • Technology Badge IconIlluminaGenomeAnalyzerIIx

Description

Sequencing of 5' ends of RNA molecules from control and exosome-depleted HeLa-S3 cells. Overall design: CAGE library construction from RNA extracted from control and exosome-depleted cells.

Publication Title

Nuclear stability and transcriptional directionality separate functionally distinct RNA species.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon SRP150408
The RNA exosome contributes to gene expression regulation during stem cell differentiation [CAGE]
  • organism-icon Mus musculus
  • sample-icon 8 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

Gene expression programs change during cellular transitions. It is well established that a network of transcription factors and chromatin modifiers regulate RNA levels during embryonic stem cell (ESC) differentiation, but the full impact of post-transcriptional processes remains elusive. While cytoplasmic RNA turnover mechanisms have been implicated in differentiation, the contribution of nuclear RNA decay has not been investigated. Here, we differentiate mouse ESCs, depleted for the ribonucleolytic RNA exosome, into embryoid bodies to determine to which degree RNA abundance in the two states can be attributed to changes in transcription vs. RNA decay by the exosome. As a general observation, we find that exosome depletion mainly leads to the stabilization of RNAs from lowly transcribed loci, including several protein-coding genes. In particular, transcripts that are differentially expressed between states tend to be more exosome sensitive in the state where expression is low. We conclude that the RNA exosome contributes to down-regulation of transcripts with disparate expression, often in conjunction with transcriptional down-regulation. Overall design: CAGE experiments were carried out in mouse embryonic stem cells and embryoid bodies differentiated for three days upon depletion of RRP40 with shRNAs, using a scrambled shRNA as control. The experiments were performed in duplicates

Publication Title

The RNA exosome contributes to gene expression regulation during stem cell differentiation.

Sample Metadata Fields

Specimen part, Cell line, Subject

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accession-icon GSE106091
Genes regulated by TTF-1 in small cell lung cancer cell lines
  • organism-icon Homo sapiens
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

To investigate genes possibly regulated by TTF-1 in small cell lung cancer cell lines, we compared gene expression profiles of NCI-H209 and Lu139 cell lines electroporated with control and TTF-1 siRNAs.

Publication Title

An integrative transcriptome analysis reveals a functional role for thyroid transcription factor-1 in small cell lung cancer.

Sample Metadata Fields

Cell line

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accession-icon GSE67022
Regulation of Rat Hepatic Translation by mTOR
  • organism-icon Rattus norvegicus
  • sample-icon 40 Downloadable Samples
  • Technology Badge Icon Affymetrix Rat Gene 1.0 ST Array (ragene10st)

Description

Our strategy was to manipulate mTOR signaling in vivo, then characterize the transcriptome and translating mRNA in liver tissue. In adult rats, we used the non-proliferative growth model of refeeding after a period of fasting, and the proliferative model of liver regeneration following partial hepatectomy. We also studied livers from pre-term fetal rats (embryonic day 19-20) in which fetal hepatocytes are asynchronously proliferating. All three models employed rapamycin to inhibit mTOR signaling.

Publication Title

Profiling of the fetal and adult rat liver transcriptome and translatome reveals discordant regulation by the mechanistic target of rapamycin (mTOR).

Sample Metadata Fields

Specimen part, Time

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accession-icon GSE97897
Engraftment and Repopulation Potential of Late Gestation Fetal Rat Hepatocytes
  • organism-icon Rattus norvegicus
  • sample-icon 9 Downloadable Samples
  • Technology Badge Icon Affymetrix Rat Gene 1.0 ST Array (ragene10st)

Description

Liver transplantation is the only therapeutic option for patients with end-stage liver disease. The shortage of donor organs has led to the search for alternative therapies to restore liver function and bridge patients to transplantation. Our previous work has shown that the proliferation of late gestation E19 fetal hepatocytes is mitogen-independent. This is manifested as differences in the control of ribosome biogenesis, global translation, cell cycle progression and gene expression. In the present study, we investigated whether E19 fetal hepatocytes would engraft and repopulate an injured adult liver.

Publication Title

Engraftment and Repopulation Potential of Late Gestation Fetal Rat Hepatocytes.

Sample Metadata Fields

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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