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accession-icon SRP053191
Cellular response to heat shock and ER stress
  • organism-icon Mus musculus
  • sample-icon 18 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

Analysis of the coordinated transcriptional reponse to heat shock and ER stress Overall design: mRNA profiles of NIH3T3 cells which stably expressing DD-sfGFP were generated by deep sequencing, in triplicate, using Illumina HiSeq. The samples were collected from indicated timepoints after exposed to either heat stress or ER stress.

Publication Title

Distinct transcriptional responses elicited by unfolded nuclear or cytoplasmic protein in mammalian cells.

Sample Metadata Fields

No sample metadata fields

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accession-icon SRP053092
Cellular response to unfolded proteins in cytosol and nucleus
  • organism-icon Mus musculus
  • sample-icon 15 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

Analysis of the coordinated transcriptional response to unfolded proteins in cytosol and nucleus utilizing mRNA-seq Overall design: mRNA profiles of NIH3T3 cells which stably expressing DD-sfGFP were generated by deep sequencing using Illumina HiSeq2000. The samples were collected from indicated timepoints after Shield-1 removal.

Publication Title

Distinct transcriptional responses elicited by unfolded nuclear or cytoplasmic protein in mammalian cells.

Sample Metadata Fields

No sample metadata fields

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accession-icon SRP006561
RNA-seq experiments in human neural crest cells (hNCC)
  • organism-icon Homo sapiens
  • sample-icon 1 Downloadable Sample
  • Technology Badge IconIlluminaGenomeAnalyzer

Description

Combining an in vitro hNCC differentiation protocol with epigenomic profiling, we provide the first whole-genome characterization of cis-regulatory elements in this highly relevant cell type. With this data at hand, we have characterized the chromatin state and dynamics of all human gene promoters during the course of NCC in vitro differentiation. Most importantly, we have identified a large cohort of active and NCC-specific enhancers, which we showed to be functionally relevant in vivo, in the context of embryonic development. Finally, through sequence analysis of the identified NCC enhancers, we uncovered the orphan nuclear receptors NR2F1 and NR2F2 as novel hNCC transcriptional regulators both in vitro and in vivo. Overall design: RNA-seq experiments in human neural crest cells (hNCC)

Publication Title

Epigenomic annotation of enhancers predicts transcriptional regulators of human neural crest.

Sample Metadata Fields

No sample metadata fields

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accession-icon SRP040451
Reorganization of enhancer patterns in transition from naïve to primed pluripotency (RNA-seq)
  • organism-icon Mus musculus
  • sample-icon 10 Downloadable Samples
  • Technology Badge IconIllumina Genome Analyzer IIx

Description

Naïve and primed pluripotency is characterized by distinct signaling requirements, transcriptomes and developmental properties, but both cellular states share key transcriptional regulators, Oct4, Sox2 and Nanog. Here we demonstrate that transition between these two pluripotent states is associated with widespread Oct4 relocalization, mirrored by global rearrangement of enhancer chromatin landscapes. Our genomic and biochemical analyses identified candidate mediators of primed state-specific Oct4 binding, including Otx2 and Zic2/3. Even in the absence of other differentiation cues, premature Otx2 overexpression is sufficient to exit the naïve state, induce transcription of a large subset of primed pluripotency-associated genes and redirect Oct4 to thousands of previously inaccessible sites. However, ability of Otx2 to engage new enhancer regions is determined by its levels, cis-encoded properties of the sites and signaling environment. Our results illuminate regulatory mechanisms underlying pluripotency and suggest that capacity of transcription factors such as Otx2 and Oct4 to function as pioneers is highly context-dependent Overall design: transcription profile of ESCs and EpiLCs to analzye changes during differentiation and the effect of Otx2 loss and overexpression on the differentiation properties

Publication Title

Reorganization of enhancer patterns in transition from naive to primed pluripotency.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE35570
Gene signature of the post-Chernobyl papillary thyroid cancer
  • organism-icon Homo sapiens
  • sample-icon 116 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Thyroid gland is among the most sensitive organs to ionizing radiation. Whether low-dose radiation-induced papillary thyroid cancer (PTC) differs from sporadic PTC is yet unknown.

Publication Title

Gene signature of the post-Chernobyl papillary thyroid cancer.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE104397
Expression data from MMTV-PyMT Induced Tumors
  • organism-icon Mus musculus
  • sample-icon 80 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430A 2.0 Array (mouse430a2)

Description

Loss of E2F transcription factos alters metastatic capacity of MMTV-PyMT tumors.

Publication Title

Histological subtypes of mouse mammary tumors reveal conserved relationships to human cancers.

Sample Metadata Fields

Disease

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accession-icon GSE39877
Expression data from skeletal muscles of flies with muscle-specific overexpression of Foxo or Mnt
  • organism-icon Drosophila melanogaster
  • sample-icon 9 Downloadable Samples
  • Technology Badge Icon Affymetrix Drosophila Genome 2.0 Array (drosophila2)

Description

Skeletal muscle senescence influences whole organism aging, yet little is known on the relay of pro-longevity signals from muscles to other tissues. We performed an RNAi screen in Drosophila for muscle-released cytokines (?myokines?) regulating lifespan and identified Myoglianin, the homolog of human Myostatin. Myoglianin is induced in skeletal muscles by the transcription factor Mnt and together they constitute an inter-organ signaling module that regulates lifespan, age-related muscle dysfunction, and protein synthesis across aging tissues. Both Mnt and Myoglianin activate already in young age the protective decline in protein synthesis that is typical of old age, while knock-down of Myoglianin impairs this process. Mechanistically, Mnt decreases the expression of nucleolar components in muscles while also decreasing nucleolar size in distant tissues via Myostatin/p38 MAPK signaling. Our results highlight a myokine-dependent inter-organ longevity pathway that coordinates nucleolar function and protein synthesis across aging tissues.

Publication Title

Intertissue control of the nucleolus via a myokine-dependent longevity pathway.

Sample Metadata Fields

Sex, Specimen part, Treatment

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accession-icon GSE57660
Novel strategies to enforce an epithelial phenotype in mesenchymal cells
  • organism-icon Homo sapiens
  • sample-icon 3 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

E-cadherin downregulation in cancer cells is associated with epithelial-to-mesenchymal transition (EMT) and metastatic prowess, but the underlying mechanisms are incompletely characterized. In this study, we probed E-cadherin expression at the plasma membrane as a functional assay to identify genes involved in E-cadherin downregulation. The assay was based on the E-cadherin-dependent invasion properties of the intracellular pathogen Listeria monocytogenes. On the basis of a functional readout, automated microscopy and computer-assisted image analysis were used to screen siRNAs targeting 7,000 human genes. The validity of the screen was supported by its definion of several known regulators of E-cadherin expression, including ZEB1, HDAC1 and MMP14. We identified three new regulators (FLASH, CASP7 and PCGF1), the silencing of which was sufficient to restore high levels of E-cadherin transcription. Additionally, we identified two new regulators (FBXL5 and CAV2), the silencing of which

Publication Title

Novel strategies to enforce an epithelial phenotype in mesenchymal cells.

Sample Metadata Fields

Age, Specimen part, Cell line, Treatment

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accession-icon GSE11887
Differential Cardiac Gene Regulation by Arg- and Gly389 Polymorphic Forms of the beta1-adrenergic Receptor
  • organism-icon Mus musculus
  • sample-icon 24 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

The beta1-adrenergic receptor (beta1AR; ADRB1) polymorphism Arg 389Gly is located in an intracellular loop and is associated with distinct human and mouse cardiovascular phenotypes. To test the hypothesis that beta1-Arg389 and beta1-Gly389 alleles could differentially couple to pathways beyond that of classic Gs-adenylyl cyclase (AC)/cAMP signaling, we performed comparative gene expression profile analyses on hearts from wildtype and transgenic mice that expressed either human beta1-Arg389 and beta1-Gly389 receptors, or AC5 adenyl cyclase, sampling at an early age and stage, prior to the onset of pathologic features. We observed substantial overlap of dysregulated genes across all three transgenic heart models, consistent with a shared coupling to cAMP-dependent regulation of cardiac processes and adaptive responses. All three models up-regulated genes associated with RNA metabolism and translation, and down-regulated genes associated with mitochondria and energy metabolism, consistent with cAMP-driven increase in cardiac contractility, protein synthesis, and compensatory down-regulation of mitochondrial energy production. Both beta1AR transgenics activated additional genes associated with kinase-dependent pathways, and uniquely, beta1-Arg389 hearts caused up-regulation of genes associated with inflammation, programmed cell death, and extracellular matrix. These results substantially expand the scope of 7-transmembrane domain receptor signaling propagation beyond known cognate G-protein couplings. Moreover, they implicate alterations of a repertoire of processes evoked by a single amino acid variation in the cardiac beta1AR that might be exploited for genotype-specific heart failure diagnostics and therapeutics.

Publication Title

Differential coupling of Arg- and Gly389 polymorphic forms of the beta1-adrenergic receptor leads to pathogenic cardiac gene regulatory programs.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE148711
Gene expression data from bladder cells treated with Escherichia coli Extracellular Vesicles RNA
  • organism-icon Homo sapiens
  • sample-icon 21 Downloadable Samples
  • Technology Badge Icon Affymetrix Clariom S Human array (clariomshuman)

Description

Escherichia coli release Extracellular Vesicles (EVs) which carry diverse molecular cargo. Pathogenic E.coli EVs contain virulence factors which assist during infection in the host in different mechanisms.The RNA cargo of E.coli EVs has not been assessed in their effect in the host. We used microarray data to asses and compare the global response of bladder cells to EV-RNA from pathogenic E.coli (Uropathogenic UPEC 536) and non-pathogenic E. coli (probiotic Nissle 1917)

Publication Title

Effect of the Extracellular Vesicle RNA Cargo From Uropathogenic <i>Escherichia coli</i> on Bladder Cells.

Sample Metadata Fields

Disease

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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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