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accession-icon GSE50530
Identification of ATF2 target genes
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

In order to identify transcriptional targets of ATF2, we used a recombinant adenovirus to express constitutively active ATF2 in murine hepatoblasts. Expression of GFP was the control condition.

Publication Title

JNK suppresses tumor formation via a gene-expression program mediated by ATF2.

Sample Metadata Fields

Specimen part

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accession-icon GSE59196
Frequent Loss-of-Function Mutations in MLK4 Suppresses Signaling in the JNK-cJUN-p21/p15 Pathway to Promote Growth of Colon Cancer Cells
  • organism-icon Homo sapiens
  • sample-icon 20 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

The goal of the study was to evaluate the influence of mutations in MLK4 on the protein function and the process of tumorigenesis in colorectal cancers. Biochemical data imply that a majority of MLK4 mutations in colon cancer are loss-of-function, including, E314K and Y330H mutations.

Publication Title

Recurrent MLK4 Loss-of-Function Mutations Suppress JNK Signaling to Promote Colon Tumorigenesis.

Sample Metadata Fields

Specimen part, Cell line

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accession-icon GSE99077
Gene Expression profiles from allograft tumours
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Recent studies have suggested increased plasticity of differentiated cells within the intestine to act both as intestinal stem cells and tumour initiating cells. However, little is known of the processes that regulate this plasticity. Our previous work has shown that activating mutations of Kras or the NF-kB pathway can drive dedifferentiation of intestinal cells lacking Apc.

Publication Title

TGFβ pathway limits dedifferentiation following WNT and MAPK pathway activation to suppress intestinal tumourigenesis.

Sample Metadata Fields

Specimen part

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accession-icon GSE99100
Gene expression profiels from organoids.
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Recent studies have suggested increased plasticity of differentiated cells within the intestine to act both as intestinal stem cells and tumour initiating cells. However, little is known of the processes that regulate this plasticity. Our previous work has shown that activating mutations of Kras or the NF-kB pathway can drive dedifferentiation of intestinal cells lacking Apc.

Publication Title

TGFβ pathway limits dedifferentiation following WNT and MAPK pathway activation to suppress intestinal tumourigenesis.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon GSE58969
Effect of fbw7 deletion in mouse pancreatic ducts
  • organism-icon Mus musculus
  • sample-icon 3 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

The adult pancreas is capable of limited regeneration after injury, but has no defined stem cell population. The cell types and molecular signals that govern the production of new pancreatic tissue are not well understood. Here we show that inactivation of the SCF-type E3 ubiquitin ligase substrate recognition component Fbw7 induces pancreatic ductal cells to reprogram into -cells. The induced -cells resemble islet -cells in morphology and histology, express genes essential for -cell function, and release insulin upon glucose challenge. Thus, loss of Fbw7 appears to reawaken an endocrine developmental differentiation program in adult pancreatic ductal cells. Our study highlights the plasticity of seemingly differentiated adult cells, identifies Fbw7 as a master regulator of cell fate decisions in the pancreas, and reveals adult pancreatic duct cells as a latent multipotent cell type.

Publication Title

Loss of Fbw7 reprograms adult pancreatic ductal cells into α, δ, and β cells.

Sample Metadata Fields

Specimen part, Treatment

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accession-icon GSE26169
Expression data for Saccharomyces cerevisiae oxidative stress response
  • organism-icon Saccharomyces cerevisiae
  • sample-icon 210 Downloadable Samples
  • Technology Badge Icon Affymetrix Yeast Genome S98 Array (ygs98)

Description

Oxidative stress is a harmful condition in a cell, tissue, or organ, caused by an imbalnace between reactive oxygen species and other oxidants and the capacity of antioxidant defense systems to remove them. The budding yeast S. cerevisiae has been the major eukaryotic model for studies of response to oxidative stress.

Publication Title

No associated publication

Sample Metadata Fields

Time

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accession-icon GSE72439
Effect of summer daylight exposure and genetic background on growth in growth hormone deficient children
  • organism-icon Homo sapiens
  • sample-icon 60 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

The response to growth hormone in humans is dependent on phenotypic, genetic and environmental factors. The present study in children with growth hormone deficiency (GHD) collected worldwide characterised gene-environment interactions on growth response to recombinant human growth hormone (r-hGH). Growth responses in children are linked to latitude, and we found that a correlation of latitude, summer daylight exposure (SDE) was a key environmental factor related to growth response to r-hGH. In turn growth response was determined by an interaction between both SDE and genes known to affect growth response to r-hGH. In addition analysis of associated networks of gene expression implicated a role for circadian clock pathways and specifically the developmental transcription factor NANOG. This work provides the first observation of gene-environment interactions in children treated with r-hGH.

Publication Title

Effect of summer daylight exposure and genetic background on growth in growth hormone-deficient children.

Sample Metadata Fields

Sex, Age

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accession-icon GSE8994
A Comparison of microarray and MPSS Technology Platforms for Expression Analysis of Arabidopsis
  • organism-icon Arabidopsis thaliana
  • sample-icon 21 Downloadable Samples
  • Technology Badge Icon Affymetrix Arabidopsis ATH1 Genome Array (ath1121501)

Description

A comparison of microarray and MPSS technologies can help to establish the metrics for data comparisons across these technology platforms and determine some of the factors affecting the measurement of mRNA abundances using different platforms. Here, different Treatments/Conditions based on different Arabidopsis tissues were used for three different platforms include MPSS, Affymetrix and Agilent.

Publication Title

A comparison of microarray and MPSS technology platforms for expression analysis of Arabidopsis.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon E-MTAB-2613
Transcription profiling by array of four strains of budding yeast with inversions engineered between TY1 elements against matching controls
  • organism-icon Saccharomyces cerevisiae
  • sample-icon 23 Downloadable Samples
  • Technology Badge Icon Affymetrix Yeast Genome 2.0 Array (yeast2)

Description

Gene expression changes due to genome region inversions was studied. Four strains of Saccharomyces cerevisiae strains with inversions engineered between TY1 elements were compared to matching controls.

Publication Title

No associated publication

Sample Metadata Fields

Subject

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accession-icon GSE39339
Expression data from glucocorticoid-treated ALL
  • organism-icon Homo sapiens
  • sample-icon 19 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Erg and AP-1 as determinants of glucocorticoid response in acute lymphoblastic leukemia.

Sample Metadata Fields

Specimen part, Disease, Disease stage, Cell line, Treatment, Subject, Time

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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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Developed by the Childhood Cancer Data Lab

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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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