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accession-icon GSE18322
Gene Expression Analysis of Ara-C Resistance in AML
  • organism-icon Mus musculus
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon

Description

Using two independently derived murine BXH2 cell lines, Ara-C resistant derivatives were developed by exposure to increasing concentrations of Ara-C. Microarray analysis comparing the Ara-C resistant cells to their Ara-C sensitive parental cell lines identified potential genes involved in Ara-C resistance.

Publication Title

Deoxycytidine kinase is downregulated in Ara-C-resistant acute myeloid leukemia murine cell lines.

Sample Metadata Fields

Specimen part, Cell line

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accession-icon GSE16389
Global analysis of gene expression by SV40 T antigen in the mouse small intestine epithelium
  • organism-icon Mus musculus
  • sample-icon 17 Downloadable Samples
  • Technology Badge Icon

Description

SV40 large T antigen (TAg) contributes to cell transformation, in part, by targeting two well characterized tumor suppressors, pRb and p53. TAg expression affects the transcriptional circuits controlled by Rb and by p53. We have performed a microarray analysis to examine the global change in gene expression induced by wild-type TAg and TAg-mutants, in an effort to link changes in gene expression to specific transforming functions. For this analysis we have used enterocytes from the mouse small intestine expressing TAg. Expression of TAg in the mouse intestine results in hyperplasia and dysplasia. Our analysis indicates that practically all gene expression regulated by TAg in enterocytes is dependent upon its binding and inactivation of the Rb-family proteins.

Publication Title

Simian virus 40 T-antigen-mediated gene regulation in enterocytes is controlled primarily by the Rb-E2F pathway.

Sample Metadata Fields

Sex, Age, Specimen part

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accession-icon GSE49089
NRASG12V oncogene mediates self-renewal in acute myelogenous leukemia
  • organism-icon Mus musculus
  • sample-icon 15 Downloadable Samples
  • Technology Badge Icon

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

NRASG12V oncogene facilitates self-renewal in a murine model of acute myelogenous leukemia.

Sample Metadata Fields

Specimen part

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accession-icon GSE10535
Retinal transcripts level alteration in the prCAD -/- mouse, a model for retinal degeneration
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon

Description

This experiment was designed to identify transcripts that exhibit changes in abundance in the context of retinal degeneration by comparing transcript levels in adult wild type and prCAD -/- mouse retinas.

Publication Title

The genomic response to retinal disease and injury: evidence for endothelin signaling from photoreceptors to glia.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE10528
The retinal transcriptional response to light damage
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon

Description

Transcriptional profiles were compared between dark adapted and light damaged BALBc (albino) mouse retinas.

Publication Title

The genomic response to retinal disease and injury: evidence for endothelin signaling from photoreceptors to glia.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE26668
Expression data from E13.5 Fz4-/-Fz8-/- and Fz4+/+Fz8-/- kidneys
  • organism-icon Mus musculus
  • sample-icon 5 Downloadable Samples
  • Technology Badge Icon

Description

Fz4 and Fz8 cooperate in regulating the branching morhpogenesis of the developing kidney during mouse embryonic development, hence determines the eventual kidney size.

Publication Title

Genetic mosaic analysis reveals a major role for frizzled 4 and frizzled 8 in controlling ureteric growth in the developing kidney.

Sample Metadata Fields

Specimen part

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accession-icon GSE59545
NF-kB in Tumor Initiation
  • organism-icon Mus musculus
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon

Description

p65-/-Ras cells show delayed tumor formation in SCID mice. However, after prolonged latency, tumor formation was observed from these mice. To understand the changes of NF-kB regulated genes before and after tumor formation, RNA from p65+/+Ras, p65+/+RasTumor, p65-/-Ras, p65-/-RasTumor cells were isolated and microarray were performed.

Publication Title

NF-κB functions in tumor initiation by suppressing the surveillance of both innate and adaptive immune cells.

Sample Metadata Fields

Specimen part

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accession-icon GSE60639
Transcriptome_Methylome_Sirt1KOESC
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Sirt1 Regulates DNA Methylation and Differentiation Potential of Embryonic Stem Cells by Antagonizing Dnmt3l.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE60500
Genomewide gene expression analysis of murine Sirt1 wild-type or knock-out embryonic stem cells (ESCs)
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon

Description

Stem-cells and transformed cancer cells specifically express a polycomb repressive complex subtype, PRC4 which characteristically contains Sirt1 (Sirtuin-1), a NAD+ dependent class III histone deacetylase (HDAC) and Eed2 isoform as specific members. Analyzing the transcriptiome and methylome analysis of Sirt1 deficient murine ESCs (Sirt1-/- ESC), we demonstrate that these cells repressed specifically on some genomic imprinted and germ-line related genes.

Publication Title

Sirt1 Regulates DNA Methylation and Differentiation Potential of Embryonic Stem Cells by Antagonizing Dnmt3l.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE41747
MEK inhibition exhibits efficacy in human and mouse neurofibromatosis tumors, despite transcriptional feedback onto ERK.
  • organism-icon Mus musculus, Homo sapiens
  • sample-icon 66 Downloadable Samples
  • Technology Badge Icon

Description

Neurofibromatosis Type 1 (NF1) patients develop benign neurofibromas and malignant peripheral nerve sheath tumors (MPNST). These incurable peripheral nerve tumors result from loss of NF1 tumor suppressor gene function, causing hyperactive Ras signaling. Activated Ras controls numerous downstream effectors, but specific pathways mediating effects of hyperactive Ras in NF1 tumors are unknown. Cross-species transcriptome analyses of mouse and human neurofibromas and MPNSTs identified global negative feedback of genes that regulate Ras-Raf- MEK- extracellular signal-regulated protein kinase (ERK) signaling in both species. Nonetheless, activation of ERK was sustained in mouse and human neurofibromas and MPNST. PD0325901, a highly selective pharmacological inhibitor of MEK, was used to test whether sustained Ras-Raf-MEK-ERK signaling contributes to neurofibroma growth in the Nf1fl/fl;Dhh-cre mouse model or in NF1 patient MPNST cell xenografts. PD0325901 treatment reduced aberrantly proliferating cells in neurofibroma and MPNST, prolonged survival of mice implanted with human MPNST cells, and shrank neurofibromas in >80% of mice tested. PD0325901 also caused effects on tumor vasculature. Our data demonstrate that deregulated Ras/ERK signaling is critical for the growth of NF1 peripheral nerve tumors and provide strong rationale for testing MEK inhibitors in NF1 clinical trials.

Publication Title

MEK inhibition exhibits efficacy in human and mouse neurofibromatosis tumors.

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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