refine.bio
  • Search
      • Normalized Compendia
      • RNA-seq Sample Compendia
  • Docs
  • About
  • My Dataset
github link
Showing
of 18 results
Sort by

Filters

Technology

Platform

accession-icon GSE33660
Direct Recruitment of Polycomb Repressive Complex 1 (PRC1) to Chromatin by Core Binding Transcription Factors
  • organism-icon Mus musculus
  • sample-icon 9 Downloadable Samples
  • Technology Badge Icon

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Direct recruitment of polycomb repressive complex 1 to chromatin by core binding transcription factors.

Sample Metadata Fields

Specimen part, Cell line

View Samples
accession-icon GSE25643
Antagonism of B cell enhancer networks by STAT5 drives leukemia and poor patient survival
  • organism-icon Mus musculus
  • sample-icon 33 Downloadable Samples
  • Technology Badge Icon

Description

The transcription factor STAT5 plays a critical role in B cell acute lymphoblastic leukemia (B-ALL). How STAT5 mediates this effect is unclear. Here we demonstrate that STAT5 activation cooperates with defects in the pre-BCR signaling components encoded by Blnk, Btk, Prkcb, Nfkb1, and Ikzf1 to initiate B-ALL. STAT5 antagonizes NF-B and IKAROS by opposing regulation of shared target genes. STAT5 binding was enriched at super-enhancers, which were associated with an opposing network of transcription factors, including PAX5, EBF1, PU.1, IRF4, and IKAROS. Patients with high ratios of active STAT5 to NF-B or IKAROS have more aggressive disease. Our studies illustrate that an imbalance of two opposing transcriptional programs drive B-ALL, and suggest that restoring the balance of these pathways may inhibit B-ALL.

Publication Title

Antagonism of B cell enhancer networks by STAT5 drives leukemia and poor patient survival.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon GSE6757
Identification of imprinted genes expressed in adult CD3+ splenocytes
  • organism-icon Mus musculus
  • sample-icon 1 Downloadable Sample
  • Technology Badge Icon

Description

Identification of imprinted genes expressed in adult CD3+ splenocytes

Publication Title

Hematopoietic reconstitution with androgenetic and gynogenetic stem cells.

Sample Metadata Fields

Sex, Age, Specimen part

View Samples
accession-icon GSE31637
Tumor Suppressor BRCA1 epigenetically controls oncogenic miRNA-155
  • organism-icon Mus musculus
  • sample-icon 3 Downloadable Samples
  • Technology Badge Icon

Description

BRCA1, a well-known breast and ovarian cancer susceptibility gene with multiple interacting partners, is predicted to have diverse biological functions. However, to date its only well-established role is in the repair of damaged DNA and cell cycle regulation. In this regard, the etiopathological study of low penetrant variants of BRCA1 provides an opportunity to uncover its other physiologically important functions. Using this rationale, we studied the R1699Q variant of BRCA1, a potentially moderate risk variant, and found that it does not impair DNA damage repair but abrogates the repression of miR-155, a bona fide oncomir. We further show that in the absence of functional BRCA1, miR-155 is up-regulated in BRCA1-deficient mouse mammary epithelial cells, human and mouse BRCA1-deficienct breast tumor cell lines as well as tumors. Mechanistically, we found that BRCA1 represses miR-155 expression via its association with HDAC2, which deacetylates H2A and H3 on the miR-155 promoter. Finally, we show that over-expression of miR-155 accelerates whereas the knockdown of miR-155 attenuates the growth of tumor cell lines in vivo. Taken together, our findings demonstrate a new mode of tumor suppression by BRCA1 and reveal miR-155 as a potential therapeutic target for BRCA1-deficient tumors.

Publication Title

Tumor suppressor BRCA1 epigenetically controls oncogenic microRNA-155.

Sample Metadata Fields

Specimen part

View Samples
accession-icon GSE31611
Expression data from embryoid body with BRCA1 mutation [mRNA]
  • organism-icon Mus musculus
  • sample-icon 3 Downloadable Samples
  • Technology Badge Icon

Description

We examined the functional significance of the R1699Q variant of human BRCA1 gene using a mouse ES cell-based assay.

Publication Title

Tumor suppressor BRCA1 epigenetically controls oncogenic microRNA-155.

Sample Metadata Fields

Specimen part

View Samples
accession-icon GSE30016
Comparison of polysomal profiles of murine adult normal, tumor, and recruited olig2 cells
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon

Description

Comparison of polysomal profiles of murine adult olig2 cortical progenitors, murine tumor olig2 cells derived from hPDGF-B-driven glioblastomas, and murine olig2 proliferative recruited glioma cells contributing to the tumor mass but not derived from the cell of origin

Publication Title

Recruited cells can become transformed and overtake PDGF-induced murine gliomas in vivo during tumor progression.

Sample Metadata Fields

Specimen part

View Samples
accession-icon GSE10765
Expression data from MALP-2-stimulated macrophages from wild-type, IRAK-2-/- and IRAK-1-/IRAK-2-/- mice
  • organism-icon Mus musculus
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon

Description

IL-1R-associated kinases (IRAKs) participate in Toll-like receptor (TLR) signal transduction. MALP-2 is a TLR2 ligand, and stimulation of macrophages with MALP-2 activates expression of various genes including proinflammatory cytokines.

Publication Title

Sequential control of Toll-like receptor-dependent responses by IRAK1 and IRAK2.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon GSE13585
Expression data from BAT and liver of the KRAP deficient mice
  • organism-icon Mus musculus
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon

Description

KRAP (Ki-ras-induced actin-interacting protein) is a cytoskeleton-associated protein and a ubiquitous protein among tissues, originally identified as a cancer-related molecule. KRAP-deficient (KRAP-/-) mice show enhanced metabolic rate, decreased adiposity, improved glucose tolerance, hypoinsulinemia and hypoleptinemia. KRAP-/- mice are also protected against high-fat diet-induced obesity and insulin resistance despite of hyperphagia.

Publication Title

Altered energy homeostasis and resistance to diet-induced obesity in KRAP-deficient mice.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon GSE13583
Expression data from liver of the KRAP deficient mice
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon

Description

KRAP (Ki-ras-induced actin-interacting protein) is a cytoskeleton-associated protein and a ubiquitous protein among tissues, originally identified as a cancer-related molecule. KRAP-deficient (KRAP-/-) mice show enhanced metabolic rate, decreased adiposity, improved glucose tolerance, hypoinsulinemia and hypoleptinemia. KRAP-/- mice are also protected against high-fat diet-induced obesity and insulin resistance despite of hyperphagia.

Publication Title

Altered energy homeostasis and resistance to diet-induced obesity in KRAP-deficient mice.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon GSE29485
Expression data from Mouse embryo
  • organism-icon Mus musculus
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon

Description

Mice lacking the function of the PcG protein CBX2 (also known as M33) show defects in gonadal, adrenal, and splenic development. In particular, XY knockout mice develop ovaries but not testes, and the gonads are hypoplastic in both sexes.

Publication Title

Cbx2, a polycomb group gene, is required for Sry gene expression in mice.

Sample Metadata Fields

Specimen part

View Samples

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)

fund-icon Fund the CCDL

Developed by the Childhood Cancer Data Lab

Powered by Alex's Lemonade Stand Foundation

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.

BSD 3-Clause LicensePrivacyTerms of UseContact