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accession-icon GSE54285
Analysis of impact of Toxoplasma effector MAF1 during Type II infection in WT MEFs and during Type I infection in WT and MAVS KO MEFs
  • organism-icon Mus musculus
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

The goals of the microarray experiment were to determine the role of MAF1, the Toxoplasma gondii mediator of host mitochondrial association, on host cell gene expression by comparing infection of WT cells with Type II and Type II:MAF1 parasites. We also explored the role of MAF1 on host cell gene expression by comparing profiles of WT and MAVS KO MEFs infected with Type I and Type Imaf1KO parasites.

Publication Title

Toxoplasma effector MAF1 mediates recruitment of host mitochondria and impacts the host response.

Sample Metadata Fields

Specimen part, Time

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accession-icon GSE109494
Microarray analysis of gene expression during ESC cell competition
  • organism-icon Mus musculus
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

A fundamental question in developmental biology is whether there are mechanisms to detect stem cells with mutations that, although not adversely affecting viability, would compromise their ability to contribute to further development. Here, we show that cell competition is a mechanism regulating the fitness of embryonic stem cells (ESCs). We find that ESCs displaying defective bone morphogenetic protein signaling or defective autophagy or that are tetraploid are eliminated at the onset of differentiation by wild-type cells. This elimination occurs in an apoptosis-dependent manner and is mediated by secreted factors. Furthermore, during this process, we find that establishment of differential c-Myc levels is critical and that c-Myc overexpression is sufficient to induce competitive behavior in ESCs. Cell competition is, therefore, a process that allows recognition and elimination of defective cells during the early stages of development and is likely to play important roles in tissue homeostasis and stem cell maintenance.

Publication Title

Competitive interactions eliminate unfit embryonic stem cells at the onset of differentiation.

Sample Metadata Fields

Specimen part

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accession-icon GSE47920
Expression data from T lymphocytes derived from T-iPS and peripheral blood
  • organism-icon Homo sapiens
  • sample-icon 11 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

T lymphocytes can be generated from T-cell-derived induced pluripotent stem cells (T-iPS). We used microarrays to better elucidate their phenotype and compare their gene expression profile to that of known lymhoid subsets from peripheral blood.

Publication Title

Generation of tumor-targeted human T lymphocytes from induced pluripotent stem cells for cancer therapy.

Sample Metadata Fields

Specimen part

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accession-icon GSE48092
Profile of Bmpr1a-/- embryonic stem cells in ESC media and N2B27
  • organism-icon Mus musculus
  • sample-icon 11 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

A fundamental question in developmental biology is whether there are mechanisms to detect stem cells with mutations that although do not adversely affect their viability, would compromise their ability to contribute to further development. Here we show that cell competition is a novel mechanism regulating the fitness of embryonic stem cells (ESCs). We find that ESCs displaying defective BMP signalling, defective autophagy or are tetraploid are eliminated at the onset of differentiation by wild-type cells. This elimination occurs in an apoptotic dependent manner and is mediated by secreted factors. Furthermore, during this process we find that establishment of differential cMyc levels is critical and that cMyc over-expression is sufficient to induce competitive behaviour in ESCs. Cell competition is therefore a process that allows recognition and elimination of defective cells during the early stages of development and is likely to play important roles in tissue homeostasis and stem cell maintenance.

Publication Title

Competitive interactions eliminate unfit embryonic stem cells at the onset of differentiation.

Sample Metadata Fields

Specimen part

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accession-icon GSE65438
The Polycomb group protein L3MBTL1 represses a SMAD5-mediated transcriptional program in human pluripotent stem cells
  • organism-icon Homo sapiens
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Epigenetic regulation of key transcriptional programs is a critical mechanism that controls hematopoietic development and thus aberrant expression patterns or mutations in epigenetic regulators occur frequently in hematologic malignancies. We demonstrate that the Polycomb protein L3MBTL1, which is monoallelically deleted in 20q- myeloid malignancies, represses the ability of stem cells to drive hematopoietic-specific transcriptional programs by regulating the expression of SMAD5 and impairing its recruitment to target regulatory regions. Indeed, knock-down of L3MBTL1 promotes the development of hematopoiesis and impairs neural cell fate in human pluripotent stem cells. We also found a role for L3MBTL1 in regulating SMAD5 target gene expression in mature hematopoietic cell populations, thereby affecting erythroid differentiation. Taken together, we have identified epigenetic priming of hematopoietic-specific transcriptional networks, which may assist in the development of therapeutic approaches for patients with anemia.

Publication Title

The polycomb group protein L3MBTL1 represses a SMAD5-mediated hematopoietic transcriptional program in human pluripotent stem cells.

Sample Metadata Fields

Cell line

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accession-icon GSE36990
Gene expression profile of PBMCs in response to metreleptin treatment at different time points.
  • organism-icon Homo sapiens
  • sample-icon 57 Downloadable Samples
  • Technology Badge Icon Affymetrix HT Human Genome U133A Array (hthgu133a)

Description

we evaluated the modulation of gene expression profile in PBMCs from patients with hypotalamic amenorrhea. We have employed whole genome microarray expression profiling as a discovery platform to identify genes differentially expressed upon metreleptin treatment at different time points, week 12, 24 and 36.

Publication Title

Selective capacity of metreleptin administration to reconstitute CD4+ T-cell number in females with acquired hypoleptinemia.

Sample Metadata Fields

Treatment, Subject

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accession-icon GSE25725
gene expression data from cep701 treated HEL cells and shPRMT5 knocking down HEL cells
  • organism-icon Homo sapiens
  • sample-icon 8 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

compare the gene expression profile between cep701 treated HEL cells with shPRMT5 knockingdown HEL cells. HEL cells contain homologous alells with mutation Jak2V617F. We found JAK2V617F can inactivate PRMT5 activity by directly phosphorylating PRMT5 through histone methylation.

Publication Title

JAK2V617F-mediated phosphorylation of PRMT5 downregulates its methyltransferase activity and promotes myeloproliferation.

Sample Metadata Fields

Cell line, Treatment

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accession-icon SRP021085
RNAseq of PRMT4KD in human cord blood derived CD34+ cells
  • organism-icon Homo sapiens
  • sample-icon 28 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

Defining the role of epigenetic regulators in normal hematopoiesis has become critically important, as recurrent mutations or aberrant expression of these genes has been identified in both myeloid and lymphoid hematological malignancies. We have found that PRMT4, a type I arginine methyltransferase, whose function in normal and malignant hematopoiesis is unknown, is overexpressed in AML patient samples. In support of an oncogenic role for PRMT4, we find that its overexpression blocks the myeloid differentiation of human stem/progenitor cells (HSPCs) while its knockdown (KD) is sufficient to induce myeloid differentiation of HSPCs and multiple AML cell lines. Although classically thought of as a co-activator, we found that PRMT4 functions to repress the expression of miR-223 in HSPCs via the methylation of RUNX1, which triggers the assembly of a multi-protein repressor complex that includes DPF2. As part of a feedback loop, PRMT4 expression is repressed post-transcriptionally by miR-223 during the normal differentiation process. These data reveal an unidentified role of PRMT4 in myeloid differentiation and its unexpected repressive role in transcriptional regulation. Furthermore, depletion of PRMT4 results in the differentiation of myeloid leukemia cells in vitro and their decrease proliferation in vivo. Thus, targeting PRMT4 holds potential as a novel therapy for acute myelogenous leukemia. Overall design: Purified human primary CD34+ cells were transduced with lentiviruses carrying PRMT4KD or scramble control shRNAs. Total RNA was extrated. RNAseq was performed to identify target genes that are regulated by PRMT4. Experiments were performed in triplicate.

Publication Title

PRMT4 blocks myeloid differentiation by assembling a methyl-RUNX1-dependent repressor complex.

Sample Metadata Fields

Specimen part, Subject

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accession-icon GSE65215
Human induced pluripotent stem cells: diploid, chr7q deletion, spontaneous chr7 correction
  • organism-icon Homo sapiens
  • sample-icon 9 Downloadable Samples
  • Technology Badge IconIllumina HumanHT-12 V4.0 expression beadchip

Description

Gene expression analysis, a) comparing isogenic karyotypically normal iPSCs to del7q-iPSCs, b) comparing del7q-iPSCs to spontaneously corrected iPSCs. The chr7q deletion results in reduced expression levels of a large number of genes in the chr7q deleted region

Publication Title

Functional analysis of a chromosomal deletion associated with myelodysplastic syndromes using isogenic human induced pluripotent stem cells.

Sample Metadata Fields

Specimen part, Cell line

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accession-icon GSE28317
Gene expression data from human CD34+ cord blood cells infected with MIGR1, MIGR1-AML1-ETO or MIGR1-AML1-ETONHR1
  • organism-icon Homo sapiens
  • sample-icon 5 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Compare the gene expression profile among human CD34+ cord blood cells infected with MIGR1, MIGR1-AML1-ETO or MIGR1-AML1-ETONHR1

Publication Title

The leukemogenicity of AML1-ETO is dependent on site-specific lysine acetylation.

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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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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