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accession-icon GSE30446
Transcription factor SOX17 overexpression in hematopoietic stem cells
  • organism-icon Mus musculus
  • sample-icon 22 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Sox17 expression confers self-renewal potential and fetal stem cell characteristics upon adult hematopoietic progenitors.

Sample Metadata Fields

Age, Specimen part, Treatment

View Samples
accession-icon GSE30444
Retroviral Sox17 over-expression adult hematopoietic stem/progenitor cells microarray
  • organism-icon Mus musculus
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

The transcription factor SOX17 is expressed by fetal, but not adult hematoipoietic stem cells (HSCs), and is required for the maintenance of fetal and neonatal, but not adult, HSCs. In the current study we show that ectopic expression of Sox17 in adult HSCs and transiently reconstituting multipotent progenitors was sufficient to confer increased self-renewal potential and the expression of fetal HSC genes including fetal HSC surface markers.

Publication Title

Sox17 expression confers self-renewal potential and fetal stem cell characteristics upon adult hematopoietic progenitors.

Sample Metadata Fields

Specimen part, Treatment

View Samples
accession-icon GSE30445
Sox17-transgenic hematopoietic stem cell microarray
  • organism-icon Mus musculus
  • sample-icon 10 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

The transcription factor SOX17 is expressed by fetal, but not adult hematoipoietic stem cells (HSCs), and is required for the maintenance of fetal and neonatal, but not adult, HSCs. In the current study we show that ectopic expression of Sox17 in adult HSCs and transiently reconstituting multipotent progenitors was sufficient to confer increased self-renewal potential and the expression of fetal HSC genes including fetal HSC surface markers.

Publication Title

Sox17 expression confers self-renewal potential and fetal stem cell characteristics upon adult hematopoietic progenitors.

Sample Metadata Fields

Age, Specimen part, Treatment

View Samples
accession-icon SRP032541
Transcriptome analysis of yeast methyltransferase mutants set5?, set1? and set5?set1?
  • organism-icon Saccharomyces cerevisiae
  • sample-icon 10 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

Purpose: Understand the synergistic relationship between the methyltransferases Set1 and Set5 in the regulation of gene expression. Methods: Total mRNA was obtained from two independent biological replicates each of wildtype (WT), set1?, set5?, SET5 Y402A and set1?set5? S. cerevisiae strains. Libraries were generated and sequenced using an Illumina HiSeq2000 platform. The sequence reads that passed quality filters were mapped using TopHat and expression levels were quantified using Cufflinks. Results: We generated FPKM expression values for each transcript and identified the differentially expressed genes using an FDR-adjusted p-value of 0.05. Subsequent data analysis was restricted to genes with fold-change greater than 1.7 relative to WT. Our results show that Set1 and Set5 have roles primarily in transcription repression. Moreover, lack of both Set1 and Set5 results in a synergistic exhacerbation of the transcriptional derepression observed in the single mutants. Further analysis revealed a specific enrichment of the Set5/Set1-repressed genes near repetitive DNA sequences of the genome. Conclusions: Our study uncovers an unexpected synergistic role of Set1 and Set5 in transcription repression of telomeric regions and Ty retrotransposons. Overall design: mRNA profiles of wildtype (WT), set1?, set5?, SET5 Y402A and set1?set5? were generated by sequencing using an Illumina HiSeq2000 platform. Two biological replicates of each strain were used.

Publication Title

Transcriptome profiling of Set5 and Set1 methyltransferases: Tools for visualization of gene expression.

Sample Metadata Fields

Cell line, Subject

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accession-icon GSE23406
Prdm16 newborn mouse (ventricular zone) VZ cells microarray
  • organism-icon Mus musculus
  • sample-icon 9 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

As Prdm16 deficiency reduces self-renewal potential and depletes neural stem cells in culture we decided to investigate the underlying molecular mechanisms of the neural stem cells depletion in the Prdm16 deficient animals. For the experiment we used Prdm16Gt(OST67423)Lex (Prdm16LacZ) genetrap mice obtained from the NIH Mutant Mouse Regional Resource Center (http://www.mmrrc.org/).

Publication Title

Prdm16 promotes stem cell maintenance in multiple tissues, partly by regulating oxidative stress.

Sample Metadata Fields

Specimen part

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accession-icon GSE33158
Scf-GFP+ cells from the bone marrow and whole bone marrow microarray
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

The HSC niche factor SCF is required for HSC maintenance. Using an Scf-GFP knockin mouse, we have identified a perivascular cell type in the bone marrow expressing high level of Scf.

Publication Title

Endothelial and perivascular cells maintain haematopoietic stem cells.

Sample Metadata Fields

Specimen part

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accession-icon GSE74459
Translation State Array Assay for C elegans IFE-1-dependent mRNAs
  • organism-icon Caenorhabditis elegans
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix C. elegans Genome Array (celegans)

Description

Relative polysomal loading changes for wild type (N2) versus ife-1(bn127) C. elegans strains

Publication Title

Spatial and temporal translational control of germ cell mRNAs mediated by the eIF4E isoform IFE-1.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon SRP168429
RNA-Seq of PreCFU-E and CFU-E progenitors from wild type and Scf mutants
  • organism-icon Mus musculus
  • sample-icon 18 Downloadable Samples
  • Technology Badge IconNextSeq 500

Description

It has been shown previously that endothelial cells and LepR+ stromal cells are the main sources of SCF in vivo in the mouse bone marrow. We tested whether SCF from endothelial cells and/or LepR+ stromal cells is important for the maintenance of hematopoietic progenitors and erythroid progenitors in mouse bone marrow by conditional deletion of Scf from these two cell types. We discovered that Scf deletion from LepR+ stromal cells, but not endothelial cells, reduced the numbers of hematopoietic progenitors and erythroid progenitors in mice. We performed RNA-Seq on PreCFU-E and CFU-E progenitors from control mice and from mice with Scf deletion from LepR+ stromal cells. We discovered that lack of SCF from LepR+ cells induces a premature differentiation of PreCFU-E and CFU-E progenitors. Overall design: Examination of gene expression profile in 2 cell tyeps from 3 different genetic backgrounds

Publication Title

Restricted Hematopoietic Progenitors and Erythropoiesis Require SCF from Leptin Receptor+ Niche Cells in the Bone Marrow.

Sample Metadata Fields

Sex, Specimen part, Subject

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accession-icon GSE45194
Oncogenic Nras has a bimodal effect on hematopoietic stem cells promoting proliferation and self-renewal
  • organism-icon Mus musculus
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Pre-leukemic mutations are thought to promote clonal expansion of hematopoietic stem cells (HSCs) by increasing self-renewal and competitiveness. However, mutations that increase HSC proliferation tend to reduce competitiveness and self-renewal potential, raising the question of how a mutant HSC can sustainably outcompete wild-type HSCs. Activating mutations in NRAS are prevalent in human myeloproliferative disease and leukemia. Here we show that a single allele of oncogenic NrasG12D increases HSC proliferation but also increases reconstituting and self-renewal potential upon serial transplantation in irradiated mice, all without immortalizing HSCs or causing leukemia in our experiments. NrasG12D also confers long-term self-renewal potential upon multipotent progenitors. To explore the mechanism by which NrasG12D promotes HSC proliferation and self-renewal we assessed HSC cell cycle kinetics using H2B-GFP label retention. We found that NrasG12D had a bimodal effect on HSCs, increasing the proliferation of some HSCs while increasing the quiescence and competitiveness of other HSCs. One signal can therefore increase HSC proliferation, competitiveness, and self-renewal through a bimodal effect that promotes proliferation in some HSCs and quiescence in others.

Publication Title

Oncogenic Nras has bimodal effects on stem cells that sustainably increase competitiveness.

Sample Metadata Fields

Specimen part

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accession-icon GSE34880
Epigenetic reprogramming in relapsed childhood ALL
  • organism-icon Homo sapiens
  • sample-icon 13 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Reversing gene expression signatures in relapsed patient may restore chemosensitivity.

Publication Title

Epigenetic reprogramming reverses the relapse-specific gene expression signature and restores chemosensitivity in childhood B-lymphoblastic leukemia.

Sample Metadata Fields

Specimen part, Disease, Disease stage, 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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