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accession-icon GSE15105
Probing gene misregulation in bodyguard, lacerata and fiddlehead mutants
  • organism-icon Arabidopsis thaliana
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Arabidopsis ATH1 Genome Array (ath1121501)

Description

Although bodyguard (bdg), lacerata (lcr) and fiddlehead (fdh) mutations affect three unrelated genes, they trigger similar effects, i.e. ectopic organ fusion, increase of cuticle permeability. After performing cutin and wax analyses on these Arabidopsis thaliana mutants, which did not coincide with the putative enzyme functions, we hypothesised that these mutations trigger a complex response which may be visible at the transcriptional level.

Publication Title

Dissection of the complex phenotype in cuticular mutants of Arabidopsis reveals a role of SERRATE as a mediator.

Sample Metadata Fields

Specimen part

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accession-icon SRP067537
Leukemia-associated activating mutation of Flt3 expands dendritic cells and alters T cell responses
  • organism-icon Mus musculus
  • sample-icon 24 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

One of the most common genetic alterations in acute myeloid leukemia is the internal tandem duplication (ITD) in the FLT3 receptor for cytokine FLT3 ligand (FLT3L). The constitutively active FLT3-ITD promotes the expansion of transformed progenitors, but also has pleiotropic effects on normal hematopoiesis. We analyzed the effect of FLT3-ITD on dendritic cells (DCs), which express FLT3 and can be expanded by FLT3L administration. We report that young pre-leukemic mice with the Flt3ITD knock-in allele manifest an expansion of all DCs including classical (cDCs) and plasmacytoid (pDCs). The expansion originated in DC progenitors, occurred in a cell-intrinsic manner and was further enhanced in Flt3ITD/ITD mice. The mutation caused the downregulation of Flt3 on the surface of DCs and reduced their responsiveness to Flt3L. Flt3ITD mice showed enhanced capacity to support T cell proliferation, including a cell-extrinsic expansion of regulatory T cells (Tregs). Accordingly, these mice restricted alloreactive T cell responses during graft-versus-host reaction, but failed to control autoimmunity in the absence of Tregs. Thus, the FLT3-ITD mutation directly affects DC development, thereby indirectly modulating T cell homeostasis and supporting Treg expansion. This effect of FLT3-ITD may subvert immunosurveillance and promote leukemogenesis in a cell-extrinsic manner. Overall design: Sorted splenic dendritic cell subsets from either Flt3+/+ or Flt3ITD/+ mice were sequenced for mRNA profiling. For each subset per genotype contains 2-3 replicates, all from independent experiments.

Publication Title

Leukemia-associated activating mutation of Flt3 expands dendritic cells and alters T cell responses.

Sample Metadata Fields

Specimen part, Cell line, Subject

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accession-icon GSE55587
Metabolic reprogramming of stromal fibroblasts through p62-mTORC1 signaling promotes inflammation and tumorigenesis
  • organism-icon Mus musculus
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

The tumor microenvironment plays a critical role in cancer progression, but the precise mechanisms by which stromal cells influence the tumor epithelium are poorly understood. The signaling adapter p62 has been implicated as a positive regulator of epithelial tumorigenesis; however, its role in the stroma is unknown. We show here that p62 levels are reduced in the stroma of several tumors. Also, orthotopic and organotypic studies demonstrate that the loss of p62 in the tumor microenvironment or stromal fibroblasts resulted in increased tumorigenesis of epithelial prostate cancer cells. The mechanism involves the regulation of cellular redox through an mTORC1/c-Myc pathway of stromal glucose and amino acid metabolism. Inhibition of the pathway by p62 deficiency results in increased stromal IL-6 production, which is required for tumor promotion in the epithelial compartment. Thus, p62 is an anti-inflammatory tumor suppressor that acts through modulation of metabolism in the tumor stroma.

Publication Title

Metabolic reprogramming of stromal fibroblasts through p62-mTORC1 signaling promotes inflammation and tumorigenesis.

Sample Metadata Fields

Specimen part

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accession-icon GSE19795
DNA methylation in progenitor cells
  • organism-icon Homo sapiens
  • sample-icon 2 Downloadable Samples
  • Technology Badge IconIllumina HumanWG-6_V2_0_R2

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Promoter DNA methylation patterns of differentiated cells are largely programmed at the progenitor stage.

Sample Metadata Fields

Specimen part

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accession-icon GSE47559
Ibf1 and Ibf2 are DNA-binding proteins required for insulator function in Drosophila
  • organism-icon Drosophila melanogaster
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Drosophila Genome 2.0 Array (drosophila2)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Ibf1 and Ibf2 are novel CP190-interacting proteins required for insulator function.

Sample Metadata Fields

Disease, Cell line

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accession-icon GSE48774
Transcriptional responses to high glucose in adipose tissue stem cells
  • organism-icon Homo sapiens
  • sample-icon 12 Downloadable Samples
  • Technology Badge IconIllumina HumanHT-12 V4.0 expression beadchip, Illumina HumanWG-6 v3.0 expression beadchip

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Epigenetic priming of inflammatory response genes by high glucose in adipose progenitor cells.

Sample Metadata Fields

Specimen part

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accession-icon GSE19773
DNA methylation in progenitor cells: expression study
  • organism-icon Homo sapiens
  • sample-icon 2 Downloadable Samples
  • Technology Badge IconIllumina HumanWG-6_V2_0_R2

Description

We surveyed DNA methylation profiles of all human RefSeq promoters in relation to gene expression and differentiation in adipose tissue, bone marrow and muscle mesenchymal progenitors, as well as in bone marrow-derived hematopoietic progenitors. We unravel strongly overlapping DNA methylation profiles between adipose stem cells (ASCs), bone marrow mesenchymal stem cells (BMMSCs) and muscle progenitor cells (MPCs), while hematopoietic progenitor cells (HPCs) are more epigenetically distant from MSCs seen as a whole. Differentiation resolves a fraction of methylation patterns common to MSCs, generating epigenetic divergence.

Publication Title

Promoter DNA methylation patterns of differentiated cells are largely programmed at the progenitor stage.

Sample Metadata Fields

Specimen part

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accession-icon GSE48773
Effect of high glucose on gene expression in ASCs
  • organism-icon Homo sapiens
  • sample-icon 9 Downloadable Samples
  • Technology Badge IconIllumina HumanHT-12 V4.0 expression beadchip

Description

The object of this study was to investigate the effect of elevated glucose concentrations (15 and 25 mM glucose) on gene expression in undifferentiated and adipogenic differentiated ASCs.

Publication Title

Epigenetic priming of inflammatory response genes by high glucose in adipose progenitor cells.

Sample Metadata Fields

Specimen part

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accession-icon GSE47557
Co-regulation analysis of CP190 and CG9740 [expression]
  • organism-icon Drosophila melanogaster
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Drosophila Genome 2.0 Array (drosophila2)

Description

Gene expression in S2 cells after CG9740 or CP190 RNAi

Publication Title

Ibf1 and Ibf2 are novel CP190-interacting proteins required for insulator function.

Sample Metadata Fields

Cell line

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accession-icon GSE48772
Basal gene expression in proliferating ASCs
  • organism-icon Homo sapiens
  • sample-icon 3 Downloadable Samples
  • Technology Badge IconIllumina HumanWG-6 v3.0 expression beadchip

Description

The aim of this study was to characterize basal gene expression for proliferating adipose tissue MSCs, cultured at normal cell culture conditions.

Publication Title

Epigenetic priming of inflammatory response genes by high glucose in adipose progenitor cells.

Sample Metadata Fields

Specimen part

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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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Developed by the Childhood Cancer Data Lab

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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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