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accession-icon GSE40605
Histone Demethylase Lsd1 Represses Hematopoietic Stem and Progenitor Cell Signatures During Blood Cell Maturation.
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Histone demethylase Lsd1 represses hematopoietic stem and progenitor cell signatures during blood cell maturation.

Sample Metadata Fields

Sex, Specimen part

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accession-icon GSE21056
Differential roles of Sall4 isoforms in ES cell pluripotency
  • organism-icon Mus musculus
  • sample-icon 8 Downloadable Samples
  • Technology Badge Icon

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Differential roles of Sall4 isoforms in embryonic stem cell pluripotency.

Sample Metadata Fields

Specimen part, Cell line

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accession-icon GSE21054
Differential roles of Sall4 isoforms in ES cell pluripotency: expression
  • organism-icon Mus musculus
  • sample-icon 8 Downloadable Samples
  • Technology Badge Icon

Description

Murine embryonic stem cells (ESCs) are defined by continuous self-renewal and pluripotency. A diverse repertoire of protein isoforms arising from alternative splicing are expressed in ES cells without defined biological roles. Sall4, a transcription factor essential for pluripotency, exists as two isoforms (Sall4a and Sall4b). By genome-wide location analysis, we have determined that Sall4b, and not Sall4a, binds preferentially to highly expressed loci in ES cells. Sall4a and Sall4b binding sites are distinguished by both epigenetic marks at target loci and their clustering with binding sites of other pluripotency factors. When ESCs expressing a single isoform of Sall4 are generated, Sall4b alone could maintain the pluripotent state, although it could not completely suppress all differentiation markers. Sall4a and Sall4b collaborate in maintenance of the pluripotent state, but play distinct roles. Our work is novel in establishing such isoform-specific differences in ES cells.

Publication Title

Differential roles of Sall4 isoforms in embryonic stem cell pluripotency.

Sample Metadata Fields

Specimen part, Cell line

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accession-icon GSE40284
Gene expression data of Lsd1fl/fl and Lsd1fl/fl Mx1Cre CD150+ CD48- lin- c-Kit+ Sca-1+ LT-HSCs
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon

Description

We discovered that mice that lack Lsd1 in hematopoietic cells were exhibited increased frequencies of CD150+ CD48- lin- c-Kit+ Sca-1+ LT-HSCs, but completely lacked the lin- c-Kit+ Sca-1- myeloid progenitor compartment. To determine the genes altered by Lsd1-loss, CD150+ CD48- lin- c-Kit+ Sca-1+ LT-HSCs from Lsd1fl/fl and Lsd1fl/fl Mx1Cre mice were FACS-purified to be analyzed by gene expression profiling.

Publication Title

No associated publication

Sample Metadata Fields

Sex, Specimen part

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accession-icon GSE19169
Jumonji modulates Polycomb activity and self-renewal versus differentiation of stem cells
  • organism-icon Mus musculus
  • sample-icon 30 Downloadable Samples
  • Technology Badge Icon

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Jumonji modulates polycomb activity and self-renewal versus differentiation of stem cells.

Sample Metadata Fields

Specimen part

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accession-icon GSE48112
BET Bromodomains Mediate Transcriptional Pause Release in Heart Failure
  • organism-icon Mus musculus, Rattus norvegicus
  • sample-icon 26 Downloadable Samples
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Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

BET bromodomains mediate transcriptional pause release in heart failure.

Sample Metadata Fields

Age, Specimen part, Treatment

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accession-icon GSE8836
CLL in Em-TCL1 mice provides a biologically relevant model to unravel and reverse immune deficiency in human cancer.
  • organism-icon Mus musculus
  • sample-icon 46 Downloadable Samples
  • Technology Badge Icon

Description

Immune deficiency is common in cancer, but the biological basis for this and ways to reverse it remains elusive. Here we present a mouse model of B cell chronic lymphocytic leukemia (CLL) that recapitulates changes in the non-malignant circulating T cells seen in patients with this illness.1 To validate this model, we examined changes in T cell gene expression, protein expression and function in Em-TCL1 transgenic mice as they developed CLL 2,3 and demonstrate that development of CLL in these transgenic mice is associated with changes in impaired T cell function and in gene expression in CD4 and CD8 T cells similar to those observed in patients with this disease. Infusion of CLL cells into non-leukemia bearing Em-TCL1 mice rapidly induces these changes, demonstrating a causal relationship between leukemia and the induction of T cell changes. This model allows dissection of the molecular changes induced in CD4 and CD8 T cells by interaction with leukemia cells and further supports the concept that cancer results in complex abnormalities in the immune microenvironment.

Publication Title

E(mu)-TCL1 mice represent a model for immunotherapeutic reversal of chronic lymphocytic leukemia-induced T-cell dysfunction.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE12982
Expression data from mouse ES cells and various differentiated cell types
  • organism-icon Mus musculus
  • sample-icon 53 Downloadable Samples
  • Technology Badge Icon

Description

We used microarrays to detail the role of Polycomb proteins including Ezh2 and Eed in maintaining ES cell identity and executing pluripotency.

Publication Title

EZH1 mediates methylation on histone H3 lysine 27 and complements EZH2 in maintaining stem cell identity and executing pluripotency.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE6610
Expression data from murine ventral prostate treated with placebo or RAD001 for 12h, 48h, 6d,9d, and 15d
  • organism-icon Mus musculus
  • sample-icon 51 Downloadable Samples
  • Technology Badge Icon

Description

A mTOR depedent and a phenotype dependent sigature can be identified.

Publication Title

No associated publication

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon GSE19693
STAR RNA-binding protein, Quaking, suppresses cancer via regulation of microRNA
  • organism-icon Mus musculus, Homo sapiens
  • sample-icon 25 Downloadable Samples
  • Technology Badge Icon

Description

MicroRNAs have emerged as major genetic elements in the genesis and suppression of cancer. Here, multi-dimensional cancer genome analysis and validation has defined a novel Glioblastoma Multiforme (GBM) tumor suppressor pathway and mechanism of action centered on Quaking (QK), a member of the STAR family of RNA-binding proteins. Combined functional, biochemical and computational studies establish that p53 directly regulates QK gene expression, QK protein binds and stabilizes miR-20a of the cancer-relevant miR-17-92 cluster, and miR-20a in turn functions to regulate TGFR2 and the TGF signaling network. Linkage of these pathway components is supported by their genome and expression status across GBM specimens and by their gain- and loss-of-function interactions in in vitro and in vivo complementation studies. This p53-QK-miR-20a axis expands our understanding of the p53 tumor suppression network in cancer and reveals a novel tumor suppression mechanism involving regulation of specific cancer-relevant microRNAs.

Publication Title

STAR RNA-binding protein Quaking suppresses cancer via stabilization of specific miRNA.

Sample Metadata Fields

Specimen part, Cell line

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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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