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accession-icon GSE2815
cMyb and vMyb in MCF7 cells
  • organism-icon Homo sapiens
  • sample-icon 7 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A Array (hgu133a)

Description

The transcriptional activities of c-Myb and its oncogenic variant v-Myb were compared by expressing them in human MCF7 cells using recombinant adenovirus vectors. A hybrid construct, 3Mutc, which is a variant of c-Myb harboring three v-Myb-derived DNA binding domain mutations was also analyzed. All the samples were compared to cells infected with a control adenovirus. The results showed that v-Myb, which differs from c-Myb only by N- and C-terminal deletions and eleven amino acid substitutions, has a qualitatively different transcriptional activity.

Publication Title

Oncogenic mutations cause dramatic, qualitative changes in the transcriptional activity of c-Myb.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon GSE2816
cMyb and vMyb in human monocytes
  • organism-icon Homo sapiens
  • sample-icon 5 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

The transcriptional activities of c-Myb and its oncogenic variant v-Myb were compared by expressing them in primary human monocytes using recombinant adenovirus vectors. All the samples were compared to cells infected with a control adenovirus expressing only GFP. The results showed that v-Myb, which differs from c-Myb only by N- and C-terminal deletions and eleven amino acid substitutions, has a qualitatively different transcriptional activity.

Publication Title

Oncogenic mutations cause dramatic, qualitative changes in the transcriptional activity of c-Myb.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon GSE14691
Transcriptional and post-transcriptional impact of toxic RNA in myotonic dystrophy
  • organism-icon Mus musculus
  • sample-icon 58 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Expression 430A Array (moe430a)

Description

Myotonic dystrophy type 1 (DM1) is an RNA dominant disease in which mutant transcripts containing an expanded CUG repeat (CUGexp) cause muscle dysfunction by interfering with biogenesis of other mRNAs. The toxic effects of mutant RNA are mediated partly through sequestration of splicing regulator Muscleblind-like 1 (Mbnl1), a protein that binds to CUGexp RNA. A gene that is prominently affected encodes chloride channel 1 (Clcn1), resulting in hyperexcitability of muscle (myotonia). To identify DM1-affected genes and study mechanisms for dysregulation, we performed global mRNA profiling in transgenic mice that express CUGexp RNA, as compared to Mbnl1 knockout and Clcn1 null mice. We found that the majority of changes induced by CUGexp RNA in skeletal muscle can be explained by reduced activity of Mbnl1, including many changes that are secondary to myotonia. The pathway most affected comprises genes involved in calcium signaling and homeostasis. Some effects of CUGexp RNA on gene expression are caused by abnormal alternative splicing or downregulation of Mbnl1-interacting mRNAs. However, several of the most highly dysregulated genes showed altered transcription, as indicated by parallel changes of the corresponding premRNAs. These results support the idea that trans-dominant effects of CUGexp RNA on gene expression in this transgenic model may occur at the level of transcription, RNA processing, and mRNA decay, and are mediated mainly but not entirely through sequestration of Mbnl1.

Publication Title

Transcriptional and post-transcriptional impact of toxic RNA in myotonic dystrophy.

Sample Metadata Fields

Sex, Age

View Samples
accession-icon GSE51062
Expression data from human GBMs
  • organism-icon Homo sapiens
  • sample-icon 45 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Analysis of human glioblastoma multiforme tumors revealed genes that are upregulated in tumors expressing EGFRvIII compared to those expressing wild-type EGFR

Publication Title

Sprouty2 Drives Drug Resistance and Proliferation in Glioblastoma.

Sample Metadata Fields

Specimen part

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accession-icon GSE51147
Expression data from rat tumors formed by 9L.EV or 9L.EGFRvIII cells
  • organism-icon Rattus norvegicus
  • sample-icon 12 Downloadable Samples
  • Technology Badge IconIllumina ratRef-12 v1.0 expression beadchip

Description

Analysis of rat tumor xenografts revealed genes that are upregulated in tumors expressing EGFRvIII

Publication Title

Sprouty2 Drives Drug Resistance and Proliferation in Glioblastoma.

Sample Metadata Fields

Sex

View Samples
accession-icon GSE57864
Gene expression in diploid and evolved tetraploid RPE-1 and BJ-1 cells
  • organism-icon Homo sapiens
  • sample-icon 11 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Both diploid RPE-1 and BJ-1 cells were made tetraploid by transient treatment with the cytokinesis inhibitor DCD. Proliferating tetraploids from both BJ-1 and RPE-1 were selected and isolated. The gene expression profiles of the proliferating tetraploid cells were then compared to the diploids from which they originated.

Publication Title

Cytokinesis failure triggers hippo tumor suppressor pathway activation.

Sample Metadata Fields

Specimen part

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accession-icon GSE75701
Human expression data from iPSCs, motor neurons derived from iPSCs and ESCs, and fetal spinal cords
  • organism-icon Homo sapiens
  • sample-icon 9 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

We compare transcriptomic profiles of human induced pluripotent stem cells (iPSCs), motor neurons (MNs) in vitro differentiated from iPSCs or human ESCs containing a HB9::GFP reporter for MNs, and human fetal spinal cords.

Publication Title

ALS disrupts spinal motor neuron maturation and aging pathways within gene co-expression networks.

Sample Metadata Fields

Sex

View Samples
accession-icon GSE10730
Analysis of Iron Deficiency in Soybean Leaf Tissue
  • organism-icon Glycine max
  • sample-icon 11 Downloadable Samples
  • Technology Badge Icon Affymetrix Soybean Genome Array (soybean)

Description

This study was designed to identify candidate genes associated with iron efficiency in soybeans. Two genotypes, Clark (PI548553) and IsoClark (PI547430), were grown in both iron sufficient (100uM Fe(NO3)3) and iron deficient (50uM Fe(NO3)3) hydroponics conditions. The second trifoliate was harvested for RNA extraction for the microarray experiment. Candidate genes were identified by comparing gene expression profiles within genotypes between the two iron growth conditions.

Publication Title

Integrating microarray analysis and the soybean genome to understand the soybeans iron deficiency response.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon GSE57769
Gene expression profile of diploid and tetraploid mouse primary hepatocyte
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430A 2.0 Array (mouse430a2)

Description

Genetically unstable tetraploid cells can promote tumorigenesis. Recent estimates suggest that ~37% of human tumors have undergone a genome-doubling event during their development. This potentially oncogenic effect of tetraploidy is countered by a p53-dependent barrier to proliferation. However, the cellular defects and corresponding signaling pathways that trigger growth suppression in tetraploid cells are not known. Here we combine genome-scale RNAi screening and in vitro evolution approaches to demonstrate that cytokinesis failure activates the Hippo tumor suppressor pathway in cultured cells as well as in naturally occurring tetraploid cells in vivo. Induction of the Hippo pathway is triggered in part by extra centrosomes, which alter small G-protein signaling and activate LATS2 kinase; LATS2 in turn stabilizes p53 and inhibits the transcriptional regulators YAP and TAZ. These findings define an important tumor suppression mechanism. Furthermore, our experiments uncover adaptations that allow nascent tumor cells to bypass this inhibitory regulation.

Publication Title

Cytokinesis failure triggers hippo tumor suppressor pathway activation.

Sample Metadata Fields

Age, Specimen part

View Samples
accession-icon GSE85846
Adipose tissue stromal cells from lean, obese, and formerly obese mice
  • organism-icon Mus musculus
  • sample-icon 24 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 2.1 ST Array (mogene21st)

Description

Adipose tissue stromal cells contribute to the regulation of adipose tissue in lean and obese states. Myeloid cells such as adipose tissue macrophages (ATMs) and dendritic cells (ATDCs) undergo both quantitative and qualitative changes with obesity. Due to similarity in markers the identify of adipose tissue dendritic cells and macrophages has been elusive. We have refined prior protocols to unambiguously discern ATM and ATDC in mice. We used microarrays to compare the profiles of ATMs and ATDC from gonadal adipose tissue from lean, obese, and formerly obese mice. We also isolated preadipocytes (PA) from lean and obese mice for comparison.

Publication Title

Adipose Tissue Dendritic Cells Are Independent Contributors to Obesity-Induced Inflammation and Insulin Resistance.

Sample Metadata Fields

Sex, Specimen part

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)

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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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