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accession-icon SRP051606
Dissection of transcriptional and cis-regulatory control of differentiation in human pancreatic cancer [RNA-seq]
  • organism-icon Homo sapiens
  • sample-icon 29 Downloadable Samples
  • Technology Badge IconIlluminaGenomeAnalyzerII

Description

The histological grade of carcinomas describes the ability of tumor cells to organize differentiated epithelial structures and has prognostic impact. Molecular control of differentiation in normal and cancer cells relies on lineage-determining transcription factors (TFs) that activate the repertoire of cis-regulatory elements controlling cell type-specific transcriptional outputs. TF recruitment to cognate genomic DNA binding sites results in the deposition of histone marks characteristic of enhancers and other cis-regulatory elements. Here we integrated transcriptomics and genome-wide analysis of chromatin marks in human pancreatic ductal adenocarcinoma (PDAC) cells of different grade to identify first, and then experimentally validate the sequence-specific TFs controlling grade-specific gene expression. We identified a core set of TFs with a pervasive binding to the enhancer repertoire characteristic of differentiated PDACs and controlling different modules of the epithelial gene expression program. Defining the regulatory networks that control the maintenance of epithelial differentiation of PDAC cells will help determine the molecular basis of PDAC heterogeneity and progression. Overall design: Poly(A) fraction of the total RNA from human pancreatic ductal adenocarcinoma cell lines was extracted and subjected to by multiparallel sequencing. Experiments were carried out in unmodified cells in duplicate, genome edited clonal CFPAC1 cells (2 KLF5-deleted CRISPR-Cas9 clones, 3 ELF3-deleted CRISPR-Cas9 clones and 2 wt clones) and CFPAC1 cells ectopically expressing ZEB1 or empty vector control (in duplicate).

Publication Title

Dissection of transcriptional and cis-regulatory control of differentiation in human pancreatic cancer.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE87483
Dnmt3a restrains mast cell inflammatory responses
  • organism-icon Mus musculus
  • sample-icon 18 Downloadable Samples
  • Technology Badge IconIllumina MouseWG-6 v2.0 expression beadchip

Description

By utilizing mast cells lacking Dnmt3a, we found that this enzyme is involved in restraining mast cell responses to stimuli, both in vitro and in vivo.

Publication Title

<i>Dnmt3a</i> restrains mast cell inflammatory responses.

Sample Metadata Fields

Sex, Specimen part, Treatment

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accession-icon GSE29962
Nutrient-dependent growth of NIH3T3 and NIH3T3 K-ras cell lines.
  • organism-icon Mus musculus
  • sample-icon 28 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Expression profiling of normal NIH3T3 and transformed NIH3T3 K-ras cell lines grown for 72 hours in optimal glucose availability (25 mM glucose) or low glucose availability (1 mM). Low glucose induces apoptosis in transformed cells as compared to normal ones.

Publication Title

Oncogenic K-Ras decouples glucose and glutamine metabolism to support cancer cell growth.

Sample Metadata Fields

Cell line, Time

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accession-icon GSE37859
Compare gene expression profiles of mouse iNSC, WT-NSC, and MEF
  • organism-icon Mus musculus
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

The iNSC cells are two clones generated from the same MEF line. Therefore, we conducted one analysis that compared the two clonal lines and a separate analysis that compared iNSC vs. NSC, iNSC vs. MEF, and NSC vs. MEF. Both were single factor ANOVAs, the first compared two

Publication Title

Direct reprogramming of mouse and human fibroblasts into multipotent neural stem cells with a single factor.

Sample Metadata Fields

Specimen part

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accession-icon SRP091544
Cooptation of tandem DNA repeats for the control of epithelial-to-mesenchymal transition [RNA-Seq]
  • organism-icon Homo sapiens
  • sample-icon 6 Downloadable Samples
  • Technology Badge IconIllumina Genome Analyzer II

Description

During normal or pathological epithelial-to-mesenchymal transition, epithelium-specific gene expression is shut down, with the DNA-binding factor ZEB1 acting as a master suppressor of epithelial identity. Here, we show that ZEB1 occupies primate-specific tandem repeats (TRs) harboring dozens of copies of its DNA-binding motif and located within genomic loci relevant for epithelial identity. Deletion of one such repeat in a quasi-mesenchymal human cancer cell line induced the reacquisition of epithelial features and phenocopied the effects of ZEB1 gene deletion. Since ZEB1 binds clustered motifs in a non-cooperative manner, changes in its nuclear concentration enable graded adjustments of TR occupancy, thus fine-tuning repression level. In addition, high motif density in TRs allows ZEB1 binding (and shutdown of epithelial programs) despite differences in chromatin organization and accessibility among epithelial cell types. Overall design: Total RNA from human pancreatic ductal adenocarcinoma cell lines was processed for multiparallel sequencing. Experiments were carried out in genome edited clonal MiaPaCa2 cells (3 ZEB1-deleted CRISPR-Cas9 clones and 3 wt clones).

Publication Title

Co-optation of Tandem DNA Repeats for the Maintenance of Mesenchymal Identity.

Sample Metadata Fields

Cell line, Subject

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accession-icon SRP060707
TET2 Regulates Mast Cell Differentiation and Proliferation through Catalytic and Non-catalytic Activities.
  • organism-icon Mus musculus
  • sample-icon 4 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

Dioxygenases of the TET family impact genome functions by converting 5-methylcytosine in DNA to 5-hydroxymethylcytosine, but the individual contribution of the three family members to differentiation and function of myeloid cells is still incompletely understood. Using cells with a deletion in the Tet2 gene, we show that TET2 contributes to the regulation of mast cell differentiation, proliferation and effector functions. The differentiation defect observed in absence of TET2 could be however completely rescued or further exacerbated by modulating TET3 activity, and it was primarily linked to dysregulated expression of the C/EBP family of transcription factors. In contrast, hyper-proliferation induced by the lack of TET2 could not be modified by TET3. Together, our data indicate the existence of both overlapping and unique roles of individual TET proteins in regulating myeloid cell gene expression, proliferation and function. Overall design: Total mRNA of FACS-sorted Kit+ FceRIa+ populations of primary bone marrow-derived mast cells (BMMCs) from Tet2-/- and Tet2+/+ animals was extracted and subjected to multiparallel sequencing.

Publication Title

TET2 Regulates Mast Cell Differentiation and Proliferation through Catalytic and Non-catalytic Activities.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE19042
Synergistic Action of LIF and Glucocorticoids on pituitary corticotrophs cell line (AtT-20)
  • organism-icon Mus musculus
  • sample-icon 24 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Expression 430A Array (moe430a)

Description

While the hypothalamo-pituitary-adrenal axis (HPA) activates a general stress response by increasing glucocorticoid (Gc) synthesis, biological stress resulting from infections triggers the inflammatory response through production of cytokines. The pituitary gland integrates some of these signals by responding to the pro-inflammatory cytokines IL6 and LIF and to a negative Gc feedback loop. The present work used whole-genome approaches to define the LIF/STAT3 regulatory network and to delineate cross-talk between this pathway and Gc action. Genome-wide ChIP-chip identified 3 449 STAT3 binding sites, whereas 2 396 genes regulated by LIF and/or Gc were found by expression profiling. Surprisingly, LIF on its own changed expression of only 85 genes but the joint action of LIF and Gc potentiated the expression of more than a thousand genes. Accordingly, activation of both LIF and Gc pathways also potentiated STAT3 and GR recruitment to many STAT3 targets. Our analyses revealed an unexpected gene cluster that requires both stimuli for delayed activation: 83% of the genes in this cluster are involved in different cell defense mechanisms. Thus, stressors that trigger both general stress and inflammatory responses lead to activation of a stereotypic innate cellular defense response.

Publication Title

Regulatory network analyses reveal genome-wide potentiation of LIF signaling by glucocorticoids and define an innate cell defense response.

Sample Metadata Fields

Specimen part, Time

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accession-icon GSE6823
The molecular basis of plant insect interactions
  • organism-icon Arabidopsis thaliana
  • sample-icon 5 Downloadable Samples
  • Technology Badge Icon Affymetrix Arabidopsis ATH1 Genome Array (ath1121501)

Description

The aim of this study is to identify Arabidopsis genes whose expression is altered by aphid feeding. An understanding of the plant aphid interaction at the level of the plant transcriptome will 1) consolidate current areas of investigation focused on the phloem composition (the aphid diet), 2) open up areas of plant aphid interactions for ourselves and other workers, 3) Contribute to understanding the use of new molecular technologies in an environmental context and 4) contribute to existing and development of novel control strategies.Our Arabidopsis/Myzus persicae system provides a valuable model for the study because of: a) the advantages of using Arabidopsis, b) The ability to use clonal insects, c) phloem feeding aphids facilitate focus on a specific cell type, d) aphid stylectomy allows collection of pure phloem sap to monitor phloem phenotype of the plant and the insect diet, e) we have techniques to monitor the reproductive performance and feeding behaviour aphids.Our strategy has been to test the function of selected genes, particularly those regulating phloem composition (the feeding site of the aphid) based on current phloem models of phloem function. Gene choice is limited the simplicity of current models of phloem aphid interaction.We propose a simple two treatment (aphid infested vs control plants) experiment that will identify novel target genes for future analysis. Arabidopsis plants (variety Columbia) will be grown in 16/8 light/dark in temperature controlled growth rooms. At growth stage 3.90, when rosette growth is complete, 10 clonal adult Myzus persicae will be caged in clip cages on the two largest leaves on each plant. Control plants will be treated identically except that the cages will be empty. Leaves will be harvested 8 h after infestation. This time point is selected as we know that 90% of aphids are plugged into the sieve element within 2h and that a 6h lag phase has period has previously been used when examining gene expression affected by wounding. In subsequent experiments we will examine time courses of expression of relevant genes using other approaches. Pooling two leaves from each of ten plants will generate the RNA sample, ensuring that expression signals are representative of the population of plants.

Publication Title

Exploring plant responses to aphid feeding using a full Arabidopsis microarray reveals a small number of genes with significantly altered expression.

Sample Metadata Fields

Specimen part

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accession-icon GSE12344
Daily Rhythm in Expression of over 600 Genes in the Rodent Pineal Gland: Dominant Role of Adrenergic/cAMP Signaling
  • organism-icon Rattus norvegicus
  • sample-icon 50 Downloadable Samples
  • Technology Badge Icon Affymetrix Rat Genome U34 Array (rgu34a), Affymetrix Rat Expression 230A Array (rae230a), Affymetrix Rat Genome 230 2.0 Array (rat2302)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Night/day changes in pineal expression of >600 genes: central role of adrenergic/cAMP signaling.

Sample Metadata Fields

Specimen part, Time

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accession-icon GSE12343
Expt. C; Daily Rhythm in Expression of >600 Genes in the Rodent Pineal Gland: Dominant Role of Adrenergic/cAMP Signaling
  • organism-icon Rattus norvegicus
  • sample-icon 32 Downloadable Samples
  • Technology Badge Icon Affymetrix Rat Genome 230 2.0 Array (rat2302), Affymetrix Rat Genome U34 Array (rgu34a)

Description

Biological processes are optimized by circadian and circannual biological timing systems. In vertebrates, the pineal gland plays an essential role in these systems by converting time into a hormonal signal, melatonin; in all vertebrates, circulating melatonin is elevated at night, independent of lifestyle. At night, sympathetic input to the pineal gland, originating from the circadian clock in the suprachiasmatic nucleus, releases norepinephrine. This adrenergic stimulation causes an elevation of cAMP, which is thought to regulate many of the dramatic changes in genes expression known to occur at night. In many aspects, the adrenergic/cAMP effects on gene expression can be recapitulated in primary organ culture.

Publication Title

Night/day changes in pineal expression of >600 genes: central role of adrenergic/cAMP signaling.

Sample Metadata Fields

Specimen part, 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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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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