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accession-icon GSE29284
Expression data from newborn mouse brain expressing a constitutively active PDGFRb
  • organism-icon Mus musculus
  • sample-icon 8 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

To identify targets of PDGFRb signaling and potentially new markers for pericyte activation, we used microarray analysis to compare gene expression in control and mutant pericytes expressing a constitutively active PDGFRb.

Publication Title

PDGFRβ signaling regulates mural cell plasticity and inhibits fat development.

Sample Metadata Fields

Specimen part

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accession-icon SRP055777
PDGF and FGF treatment in E13.5 MEPMs II
  • organism-icon Mus musculus
  • sample-icon 22 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

PDGF and FGF treatment in E13.5 MEPMs. 4 hr PDGF treated MEPMs (3 replicates), 4 hr FGF treated MEPMs (3 replicates), 1 hr PDGF + PD325901 treated MEPMs (2 replicates), 4 hr PDGF + PD325901 treated MEPMs (2 replicates), 1 hr FGF + PD325901 treated MEPMs (2 replicates), 4 hr FGF + PD325901 treated MEPMs (2 replicates), 1 hr PDGF + LY294002 treated MEPMs (2 replicates), 4 hr PDGF + LY294002 treated MEPMs (2 replicates), 1 hr FGF + LY294002 treated MEPMs (2 replicates), 4 hr FGF + LY294002 treated MEPMs (2 replicates) Overall design: 4 hr PDGF treated MEPMs (3 replicates), 4 hr FGF treated MEPMs (3 replicates), 1 hr PDGF + PD325901 treated MEPMs (2 replicates), 4 hr PDGF + PD325901 treated MEPMs (2 replicates), 1 hr FGF + PD325901 treated MEPMs (2 replicates), 4 hr FGF + PD325901 treated MEPMs (2 replicates), 1 hr PDGF + LY294002 treated MEPMs (2 replicates), 4 hr PDGF + LY294002 treated MEPMs (2 replicates), 1 hr FGF + LY294002 treated MEPMs (2 replicates), 4 hr FGF + LY294002 treated MEPMs (2 replicates)

Publication Title

Receptor tyrosine kinases modulate distinct transcriptional programs by differential usage of intracellular pathways.

Sample Metadata Fields

No sample metadata fields

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accession-icon SRP047489
PDGF and FGF treatment in E13.5 MEPMs
  • organism-icon Mus musculus
  • sample-icon 11 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000, Illumina Genome Analyzer IIx

Description

Receptor tyrosine kinase signaling is critical for mammalian craniofacial development, but the key downstream transcriptional effectors remain unknown. We demonstrate that SRF is induced by both PDGF and FGF signaling in mouse embryonic palatal mesenchyme cells, and Srf neural crest conditional mutants exhibit facial clefting accompanied by proliferation and migration defects. Srf and Pdgfra mutants interact genetically in craniofacial development, but Srf and Fgfr1 mutants do not. This signal specificity is recapitulated at the level of cofactor activation: while both PDGF and FGF target gene promoters show enriched genome-wide overlap with SRF ChIP-seq peaks, PDGF selectively activates a network of MRTF-dependent cytoskeletal genes. Collectively, our results identify a novel role for SRF in proliferation and migration during craniofacial development and delineate a mechanism of receptor tyrosine kinase specificity mediated through differential cofactor usage, leading to a unique PDGF-responsive SRF-driven transcriptional program in the midface. Overall design: Serum Starved MEPMs (4 replicates), 1 hr PDGF treated MEPMs (4 replicates), 1 hr FGF treated MEPMs (3 replicates)

Publication Title

Receptor tyrosine kinases modulate distinct transcriptional programs by differential usage of intracellular pathways.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE20607
Genome-wide expression profiles of primary human SAECs infected with different adenovirus mutants.
  • organism-icon Homo sapiens
  • sample-icon 17 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Exon 1.0 ST Array [transcript (gene) version (huex10st)

Description

Full title: Genome-wide expression profiles of primary human small airway epithelial cells (SAECs) infected with different adenovirus mutants.

Publication Title

Heterochromatin silencing of p53 target genes by a small viral protein.

Sample Metadata Fields

Specimen part

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accession-icon GSE4271
Molecular subclasses of high-grade glioma: prognosis, disease progression, and neurogenesis
  • organism-icon Homo sapiens
  • sample-icon 200 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A Array (hgu133a)

Description

Novel prognostic subclasses of high-grade astrocytoma are identified and discovered to resemble stages in neurogenesis. One tumor class displaying neuronal lineage markers shows longer survival, while two tumor classes enriched for neural stem cell markers display equally short survival. Poor prognosis subclasses exhibit either markers of proliferation or of angiogenesis and mesenchyme. Analysis of gene expression data is described in Phillips et al., Cancer Cell, 2006.

Publication Title

Molecular subclasses of high-grade glioma predict prognosis, delineate a pattern of disease progression, and resemble stages in neurogenesis.

Sample Metadata Fields

Sex, Age, Disease stage

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accession-icon SRP065559
A designed inhibitor of p53 aggregation rescues p53 tumor-suppression in ovarian carcinomas
  • organism-icon Homo sapiens
  • sample-icon 24 Downloadable Samples
  • Technology Badge IconIlluminaHiSeq2000

Description

Half of all human cancers lose p53 function by missense mutations, with an unknown fraction of these containing p53 in a self-aggregated, amyloid-like state. Here we show that a cell-penetrating peptide, ReACp53, designed to inhibit p53 amyloid formation, rescues p53 function in cancer cell lines and in organoids derived from high-grade serous ovarian carcinomas (HGSOC), an aggressive cancer characterized by ubiquitous p53 mutations. Rescued p53 behaves similarly to its wild-type counterpart in regulating target genes, reducing cell proliferation and increasing cell death. Intraperitoneal administration decreases tumor proliferation and shrinks xenografts in vivo. Our data show the effectiveness of targeting a specific aggregation defect of p53 and its potential applicability to HGSOCs. Overall design: Vehicle vs. ReACp53 treatment in 4 different samples: 2 cell lines (MCF7 w/ WT p53 as negative control and OVCAR3 w/ R248Q p53) and 2 clinical specimens (primary cells from patient #8 w/ WT p53 as negative control and primary cells from patient #1 w/ R248Q p53)

Publication Title

A Designed Inhibitor of p53 Aggregation Rescues p53 Tumor Suppression in Ovarian Carcinomas.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE16534
Exon array profiling detects EML4-ALK fusion in breast, colorectal and non-small cell lung cancers.
  • organism-icon Homo sapiens
  • sample-icon 150 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Exon 1.0 ST Array [probe set (exon) version (huex10st)

Description

Exon array profiling of human primary tumor tissue samples including breast, colon and NSCLC.

Publication Title

Exon array profiling detects EML4-ALK fusion in breast, colorectal, and non-small cell lung cancers.

Sample Metadata Fields

Specimen part

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accession-icon GSE5901
Expression profiling of the mouse prostate after castration and hormone replacement
  • organism-icon Mus musculus
  • sample-icon 20 Downloadable Samples
  • Technology Badge Icon Affymetrix Murine Genome U74A Version 2 Array (mgu74av2)

Description

In this study, we used microarray analysis to determine gene expression profile changes in the mouse prostate following castration and hormone replacement. We first identified genes with significant expression changes in each of these two processes and then generated a list of androgen responsive genes and a list of genes whose expression were inversely correlated with the presence of androgen. The analysis of this data set is described in Wang et al., Differentiation, 2006

Publication Title

Expression profiling of the mouse prostate after castration and hormone replacement: implication of H-cadherin in prostate tumorigenesis.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE11967
Identifying alternative hyper-splicing signatures in MG-thymoma by exon arrays
  • organism-icon Homo sapiens
  • sample-icon 8 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Exon 1.0 ST Array [transcript (gene) version (huex10st)

Description

Background: The vast majority of human genes (.70%) are alternatively spliced. Although alternative pre-mRNA processing is modified in multiple tumors, alternative hyper-splicing signatures specific to particular tumor types are still lacking. Here, we report the use of Affymetrix Human Exon Arrays to spot hyper-splicing events characteristic of myasthenia gravis (MG)-thymoma, thymic tumors which develop in patients with MG and discriminate them from colon cancer changes. Methodology/Principal Findings: We combined GO term to parent threshold-based and threshold-independent ad-hoc functional statistics with in-depth analysis of key modified transcripts to highlight various exon-specific changes. These denote alternative splicing in MG-thymoma tumors compared to healthy human thymus and to in-house and Affymetrix datasets from colon cancer and healthy tissues. By using both global and specific, term-to-parent Gene Ontology (GO) statistical comparisons, our functional integrative ad-hoc method allowed the detection of disease-relevant splicing events. Conclusions/Significance: Hyper-spliced transcripts spanned several categories, including the tumorogenic ERBB4 tyrosine kinase receptor and the connective tissue growth factor CTGF, as well as the immune function-related histocompatability gene HLA-DRB1 and interleukin (IL)19, two muscle-specific collagens and one myosin heavy chain gene; intriguingly, a putative new exon was discovered in the MG-involved acetylcholinesterase ACHE gene. Corresponding changes in spliceosome composition were indicated by co-decreases in the splicing factors ASF/SF2 and SC35. Parallel tumor-associated changes occurred in colon cancer as well, but the majority of the apparent hyper-splicing events were particular to MGthymoma and could be validated by Fluorescent In-Situ Hybridization (FISH), Reverse TranscriptionPolymerase Chain Reaction (RT-PCR) and mass spectrometry (MS) followed by peptide sequencing. Our findings demonstrate a particular alternative hyper-splicing signature for transcripts over-expressed in MG-thymoma, supporting the hypothesis that alternative hyper-splicing contributes to shaping the biological functions of these and other specialized tumors and opening new venues for the development of diagnosis and treatment approaches

Publication Title

Identifying alternative hyper-splicing signatures in MG-thymoma by exon arrays.

Sample Metadata Fields

Sex

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accession-icon GSE29072
Zebularine effect on mouse embryonic stem cells manifested as cardiod-myogenic potential: testable hypothesis generation using microarray data
  • organism-icon Mus musculus
  • sample-icon 17 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Lineage commitment during Embryonic Stem Cells (ESCs) differentiation is controlled not only by a gamut of transcription factors but also by epigenetic events, mainly histone deacetylation and promoter DNA methylation. Moreover, the DNA demethylation agent 5-Aza-2-deoxycytidine (AzadC) has been widely described in the literature as an effective chemical stimulus used to promote cardiomyogenic differentiation in various stem cell types; however, its toxicity and instability complicate its use. Thus, the purpose of this study was to examine the effects of zebularine, a stable and non-toxic DNA cytosine methylation inhibitor, on ESCs differentiation. Herein are the Affymetrix Expression data obtained from RNA of murine ESCs treated with zebularine.

Publication Title

Zebularine regulates early stages of mESC differentiation: effect on cardiac commitment.

Sample Metadata Fields

Specimen part, Cell line, Treatment

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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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