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accession-icon GSE25825
Expression data from MxCre;E2F1-/-2-/-3f/f Cd11B myeloid cells
  • organism-icon Mus musculus
  • sample-icon 5 Downloadable Samples
  • Technology Badge Icon

Description

To understand the underlying cause for the observed apoptosis in E2f1-3 deficient myeloid cells. We compared gene expression profiles of Cd11b+ sorted myeloid cells isolated from bone marrow of control (E2F1-/- ) and experimental (Mxcre;E2F1-/-2-/-3f/f ) mice.

Publication Title

E2f1-3 are critical for myeloid development.

Alternate Accession IDs

E-GEOD-25825

Sample Metadata Fields

Age, Specimen part

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accession-icon GSE16454
Gene expression data from small intestines
  • organism-icon Mus musculus
  • sample-icon 23 Downloadable Samples
  • Technology Badge Icon

Description

Rb and E2F are thought to play antagonistic roles in celll proliferation. However, this model is based mostly from in vitro cell culture systems. We used small intestines to test this model in vivo.

Publication Title

E2f1-3 switch from activators in progenitor cells to repressors in differentiating cells.

Alternate Accession IDs

E-GEOD-16454

Sample Metadata Fields

Age, Specimen part

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accession-icon GSE32355
E2f7/E2f8 and E2f1/E2f2/E2f3 null and wild type liver along with E2f7/E2f8 null and wild type trophoblast giant cells
  • organism-icon Mus musculus
  • sample-icon 101 Downloadable Samples
  • Technology Badge Icon

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Canonical and atypical E2Fs regulate the mammalian endocycle.

Alternate Accession IDs

E-GEOD-32355

Sample Metadata Fields

Age, Specimen part

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accession-icon GSE32354
Expression data from E2f7/E2f8 and E2f1/E2f2/E2f3 null liver (Affymetrix)
  • organism-icon Mus musculus
  • sample-icon 35 Downloadable Samples
  • Technology Badge Icon

Description

To understand the underlying cause and mechanisms of changes in hepatocyte ploidy upon Albumin-Cre mediated deletion of E2f7&8 and Mx1-Cre mediated deletion of E2f1,2&3, we analysed global gene expression of 6 weeks and 2 months liver tissues.

Publication Title

Canonical and atypical E2Fs regulate the mammalian endocycle.

Alternate Accession IDs

E-GEOD-32354

Sample Metadata Fields

Age, Specimen part

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accession-icon GSE12601
Development and Diversification of Retinal Amacrine Interneurons at Single Cell Resolution
  • organism-icon Mus musculus
  • sample-icon 26 Downloadable Samples
  • Technology Badge Icon

Description

The vertebrate retina uses diverse neuronal cell types arrayed into complex neural circuits to extract, process and relay information from the visual scene to the higher order processing centers of the brain. Amacrine cells, a diverse class of inhibitory interneurons, are thought to mediate the majority of the processing of the visual signal that occurs within the retina. Despite morphological characterization, the number of known molecular markers of amacrine cell types is still much smaller than the 26 morphological types that have been identified. Furthermore, it is not known how this diversity arises during development. Here, we have combined in vivo genetic labeling and single cell genome-wide expression profiling to: 1) Identify specific molecular types of amacrine cells; 2) Demonstrate the molecular diversity of the amacrine cell class.

Publication Title

Development and diversification of retinal amacrine interneurons at single cell resolution.

Alternate Accession IDs

E-GEOD-12601

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE23700
HOP homeobox (Hopx) and Histone deacetylase-2 (Hdac2) deficiency effect on the embryonic heart
  • organism-icon Mus musculus
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon

Description

Analysis of heart ventricles from Hopx, Hdac2, and both Hopx-Hdac2 deficient embryos at embryonic day E16.5. Results provide insight into the role of Hopx and Hdac2 in cardiac development.

Publication Title

Hopx and Hdac2 interact to modulate Gata4 acetylation and embryonic cardiac myocyte proliferation.

Alternate Accession IDs

E-GEOD-23700

Sample Metadata Fields

Specimen part

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accession-icon GSE12599
Transcriptional profiling of mouse glomerulus in lipopolysaccharide-induced proteinuria model
  • organism-icon Mus musculus
  • sample-icon 10 Downloadable Samples
  • Technology Badge Icon

Description

The pathogenic mechanisms of common kidney glomerular diseases, including the vast majority of cases of proteinuria, remain unknown.

Publication Title

Glomerular transcriptome changes associated with lipopolysaccharide-induced proteinuria.

Alternate Accession IDs

E-GEOD-12599

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE17160
Regulatory mechanisms of TSG-6 (TNF-alfa-induced protein-6: Tnfip6)-deficient and wild-type synovial fibroblasts
  • organism-icon Mus musculus
  • sample-icon 42 Downloadable Samples
  • Technology Badge Icon

Description

BALB/c mice are susceptible to proteoglycan (PG) aggrecan-induced arthritis (PGIA), and the absence of TSG-6 further increases susceptibility and local inflammatory reactions, including neutrophil invasion into the joints. To gain insight into the mechanisms of TSG-6 action, synovial fibroblasts were isolated from wild-type and TSG-6-KO mice, cultured and exposed to various agents affecting either the TSG-6 expression and/or modify the intracellular function of TSG-6.

Publication Title

TSG-6 protein, a negative regulator of inflammatory arthritis, forms a ternary complex with murine mast cell tryptases and heparin.

Alternate Accession IDs

E-GEOD-17160

Sample Metadata Fields

Sex, Treatment

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accession-icon GSE19793
MyD88-mediated signaling prevents development of adenocarcinomas of the colon via interleukin-18
  • organism-icon Mus musculus
  • sample-icon 20 Downloadable Samples
  • Technology Badge Icon

Description

Inflammation has pleiotropic effects on carcinogenesis and tumor progression. Signaling through the adaptor protein MyD88 promotes carcinogenesis in several chemically induced cancer models. Interestingly, we observed a protective role for MyD88 in the development of AOM/DSS colitis-associated cancer. The inability of Myd88-/- mice to heal ulcers generated upon injury creates an inflammatory environment that increases the frequency of mutations and results in a dramatic increase in adenoma formation and cancer progression. Susceptibility to colitis development and enhanced polyp formation were also observed in Il18-/- mice upon AOM/DSS treatment, suggesting that the phenotype of MyD88 knockouts is in part due to their inability to signal through the IL-18 receptor. This study revealed a previously unknown level of complexity surrounding MyD88 activities downstream of different receptors that differentially impact tissue homeostasis and carcinogenesis.

Publication Title

MyD88-mediated signaling prevents development of adenocarcinomas of the colon: role of interleukin 18.

Alternate Accession IDs

E-GEOD-19793

Sample Metadata Fields

Specimen part, Disease, Disease stage

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accession-icon GSE30457
Dissecting primary (translation independent) from secondary (translation dependent) IFN-mediated differential gene expression
  • organism-icon Mus musculus
  • sample-icon 2 Downloadable Samples
  • Technology Badge Icon

Description

NIH-3T3 cells were pretreated for 15 min with either DMSO (mock) or cycloheximide followed by addition of either mock, 100 U/ml IFNalpha or 100 U/ml IFNgamma for 1h. During the last 30 min, 500 M 4-thiouridine was added to cell culture medium. Total cellular RNA was isolated using Trizol reagent and nascent RNA was purified as described (Dlken et al. RNA 2008) . Three replicates of nascent RNA were analyzed by Affymetrix Mouse Gene ST 1.0 arrays

Publication Title

Deciphering the modulation of gene expression by type I and II interferons combining 4sU-tagging, translational arrest and in silico promoter analysis.

Alternate Accession IDs

E-GEOD-30457

Sample Metadata Fields

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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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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