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accession-icon GSE34006
Role of Adenosine 2A Receptors (A2AR) on regulatory T cells (Tregs)
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

The adenosine 2A receptor (A2AR) is expressed on regulatory T cells (Tregs), but the functional significance is currently unknown. We compared the gene expression between wild-type (WT) and A2AR knockout (KO) Tregs and between WT Tregs treated with vehicle or a selective A2AR agonist.

Publication Title

Autocrine adenosine signaling promotes regulatory T cell-mediated renal protection.

Sample Metadata Fields

Specimen part

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accession-icon GSE41386
Role of REST in the pathogenesis of uterine fibroids
  • organism-icon Homo sapiens
  • sample-icon 9 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

The loss of REST in uterine fibroids promotes aberrant gene expression and enables mTOR pathway activation

Publication Title

Loss of the repressor REST in uterine fibroids promotes aberrant G protein-coupled receptor 10 expression and activates mammalian target of rapamycin pathway.

Sample Metadata Fields

Specimen part, Treatment

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accession-icon GSE9199
Synergistic response to oncogenic mutations defines gene class critical to cancer phenotype
  • organism-icon Mus musculus
  • sample-icon 50 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Understanding the molecular underpinnings of cancer is of critical importance to developing targeted intervention strategies. Identification of such targets, however, is notoriously difficult and unpredictable. Malignant cell transformation requires the cooperation of a few oncogenic mutations that cause substantial reorganization of many cell features and induce complex changes in gene expression patterns. Genes critical to this multi-faceted cellular phenotype thus only have been identified following signaling pathway analysis or on an ad hoc basis. Our observations that cell transformation by cooperating oncogenic lesions depends on synergistic modulation of downstream signaling circuitry suggest that malignant transformation is a highly cooperative process, involving synergy at multiple levels of regulation, including gene expression. Here we show that a large proportion of genes controlled synergistically by loss-of-function p53 and Ras activation are critical to the malignant state. Remarkably, 14 among 24 such 'cooperation response genes' (CRGs) were found to contribute to tumor formation in gene perturbation experiments. In contrast, only one in 14 perturbations of genes responding in a non-synergistic manner had a similar effect. Synergistic control of gene expression by oncogenic mutations thus emerges as an underlying key to malignancy and provides an attractive rationale for identifying intervention targets in gene networks downstream of oncogenic gain and loss-of-function mutations.

Publication Title

Synergistic response to oncogenic mutations defines gene class critical to cancer phenotype.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE29515
The transcriptional program controlled by Runx1 during early hematopoietic development
  • organism-icon Mus musculus
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

The transcriptional programme controlled by Runx1 during early embryonic blood development.

Sample Metadata Fields

Specimen part, Cell line

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accession-icon GSE29112
The transcriptional program controlled by Runx1 during early hematopoietic development (expression data)
  • organism-icon Mus musculus
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Transcription factors have long been recognised as powerful regulators of mammalian development, yet it is largely unknown how individual key regulators operate within wider regulatory networks. Here we have used a combination of global gene expression and chromatin-immunoprecipitation approaches across four ES-cell-derived populations of increasing haematopoietic potential to define the transcriptional programme controlled by Runx1, an essential regulator of blood cell specification. Integrated analysis of these complementary genome-wide datasets allowed us to construct a global regulatory network model, which suggested that core regulatory circuits are activated sequentially during blood specification, but will ultimately collaborate to control many haematopoietically expressed genes. Using the CD41/integrin alpha 2b gene as a model, cellular and in vivo studies showed that CD41 is controlled by both early and late circuits in fully specified blood cells, but initiation of CD41 expression critically depends on a later subcircuit driven by Runx1. Taken together, this study represents the first global analysis of the transcriptional programme controlled by any key haematopoietic regulator during the process of early blood cell specification. Moreover, the concept of interplay between sequentially deployed core regulatory circuits is likely to represent a design principle widely applicable to the transcriptional control of mammalian development.

Publication Title

The transcriptional programme controlled by Runx1 during early embryonic blood development.

Sample Metadata Fields

Specimen part, Cell line

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accession-icon SRP133849
Unique features and clinical importance of acute alloreactive immune responses
  • organism-icon Homo sapiens
  • sample-icon 24 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

By 2 weeks after stem cell transplantation, there was differentiated changes in T cell phenotype between autograft and allograft. RNA-seq was used to reveal the different transcription profiles of these T cells at week 2 after SCT. Overall design: Compare the transcription profile of the T cells in allograft and autograft transplantation patients.

Publication Title

Unique features and clinical importance of acute alloreactive immune responses.

Sample Metadata Fields

Specimen part, Disease, Subject, Time

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accession-icon SRP153814
Dissecting the autonomy of the liver circadian clock
  • organism-icon Mus musculus
  • sample-icon 54 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

The mammalian circadian clock system is made up of individual cell and tissue clocks that function as a coherent network, however it remains unclear which rhythmic functions of the liver clock are autonomous or rely on clocks in other tissues. Here, using mice which only have a functioning liver clock, we investigate the autonomous vs non-autonomous reatures of the liver clock and diurnal rhythmicity in the liver Overall design: 8-12 week-old, female WT, KO and Liver-RE BMAL1-stop-FL mice (see referenced paper for details) were fed ad libitum normal chow under 12hr light/ 12hr dark schedule. Livers were harvested every 4 hours over the circadian cycle at ZT0, 4, 8, 12, 16, 20 (n=3 per time point per group). Total RNA was extracted and used for RNA-seq.

Publication Title

Defining the Independence of the Liver Circadian Clock.

Sample Metadata Fields

Specimen part, Subject

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accession-icon GSE49787
Expression data of leukemia samples taken from transgenic ERG mice
  • organism-icon Mus musculus
  • sample-icon 9 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

The Ets transcription factor, ERG, plays a central role in definitive hematopoiesis and its overexpression in acute myeloid leukemia is associated with a stem cell signature and bad prognosis. However, little is known about the underlying mechanism by which ERG causes leukemia. Therefore we sought to identify ERG targets that participate in development of leukemia by integration of expression arrays and Chromatin immunoprecipitation.

Publication Title

Genome-scale expression and transcription factor binding profiles reveal therapeutic targets in transgenic ERG myeloid leukemia.

Sample Metadata Fields

No sample metadata fields

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accession-icon SRP091444
The pioneer factor OCT4 requires the chromatin remodeller BRG1 to support gene regulatory element function in mouse embryonic stem cells [RNA-Seq]
  • organism-icon Mus musculus
  • sample-icon 60 Downloadable Samples
  • Technology Badge IconNextSeq 500

Description

Pioneer transcription factors are able to recognise and bind their motif sequences in inaccessible or closed chromatin, and their ability to achieve this is required to establish new regulatory elements and transcriptional networks during development and cellular reprogramming. An essential feature of this pioneering activity is the transition from inaccessible chromatin to a nucleosome-depleted and accessible chromatin state typical of normal regulatory elements, and this is believed to facilitate further transcription factor binding events. However, the mechanisms by which many pioneer transcription factors achieve this remarkable feat remain elusive. Here we reveal that the pluripotency-associated pioneer factor OCT4 binds inaccessible chromatin to shape the chromatin accessibility, transcription factor co-binding and regulatory potential of thousands of distal regulatory elements in mouse embryonic stem cells, demonstrating that its pioneering activity is a feature of normal pluripotency, and not just reprogramming. The accessible chromatin formed at OCT4 binding sites relies on the chromatin remodelling factor BRG1, which is recruited to these sites by OCT4. The occupancy of BRG1 is then required to support OCT4/SOX2 co-binding and normal expression of the pluripotency-associated transcriptome, and this reliance on BRG1 reflects OCT4 binding dynamics during cellular reprograming and early mouse development. Together these observations reveal a distinct requirement for the chromatin remodelling factor BRG1 in shaping the pioneering activity of OCT4 and regulating the pluripotency network in embryonic stem cells. Overall design: ZHBTC4 and Brg1fl/fl mouse embryonic stem cells were used to ablate OCT4 and BRG1 expression respectively, followed by ATAC-seq, ChIP-seq or RNA-seq to examine their contribution towards chromatin accessibility, transcription factor occupancy, and gene expression.

Publication Title

The pioneer factor OCT4 requires the chromatin remodeller BRG1 to support gene regulatory element function in mouse embryonic stem cells.

Sample Metadata Fields

Cell line, Treatment, Subject

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accession-icon SRP065355
Small RNA and mRNA expression profiling during zebrafish caudal fin regeneration
  • organism-icon Danio rerio
  • sample-icon 54 Downloadable Samples
  • Technology Badge IconIlluminaHiSeq2500, IlluminaHiSeq2000

Description

Previous studies of zebrafish caudal fin regeneration have shown that multiple genetic programs are moduled through regulatory factors. MicroRNAs are short highly conserved non-coding genes that suppress expression of target genes and thereby control multiple genetic programs. Given their important regulatory roles and evolutionary conservation, we hypothesize that microRNAs define a conserved genetic regulatory circuit important for appendage regeneration. We characterized microRNA expression during zebrafish caudal fin regeneration using small RNA sequencing. The stages of caudal fin regeneration were assayed for mRNA expression using mRNA sequencing. Overall design: Small RNA and mRNA gene expression profiling during 0 and 4 days post amputation.

Publication Title

A Conserved MicroRNA Regulatory Circuit Is Differentially Controlled during Limb/Appendage Regeneration.

Sample Metadata Fields

No sample metadata fields

View Samples
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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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