refine.bio
  • Search
      • Normalized Compendia
      • RNA-seq Sample Compendia
  • Docs
  • About
  • My Dataset
github link
Showing
of 1163 results
Sort by

Filters

Organism

Technology

Platform

accession-icon GSE84767
Genetics of the hippocampal transcriptome in mouse: a systematic survey and online neurogenomics resource
  • organism-icon Mus musculus
  • sample-icon 67 Downloadable Samples
  • Technology Badge Icon

Description

The Hippocampus Consortium data set provides estimates of mRNA expression in the adult hippocampus of 99 genetically diverse strains of mice including 67 BXD recombinant inbred strains, 13 CXB recombinant inbred strains, a diverse set of common inbred strains, and two reciprocal F1 hybrids.

Publication Title

Genetics of the hippocampal transcriptome in mouse: a systematic survey and online neurogenomics resource.

Alternate Accession IDs

E-GEOD-84767

Sample Metadata Fields

Sex, Age, Specimen part

View Samples
accession-icon GSE7657
Identification of phase-specific arthritis-related genes in mice
  • organism-icon Mus musculus
  • sample-icon 11 Downloadable Samples
  • Technology Badge Icon

Description

Rheumatoid arthritis (RA), one of the most common polygenic diseases, is characterized by a chronic, progressive inflammation mainly in joints and has an unknown etiology. Numerous studies have revealed the significance of cytokines TNF and IL-1 in the onset and progression of RA. Due to the complexity of interactions among different cytokines and immune cells, little is known about the precise molecular mechanisms underlying RA. In this study, oligonucleotide microarray analysis and a mouse model of RA, IL-1 receptor antagonist deficient mice were used to address this issue. Two hundred and ninety transcripts were found to be dysregulated greater than or equal to 2-fold in the diseased mice. Phase-specific gene expression changes were identified, including early increase and late decrease of heat shock protein coding genes and Cyr61. Moreover, common gene expression changes were also observed, especially the upregulation of paired-Ig-like receptor A (Pira) in both early and late phases of arthritis. We conclude that common and distinct gene expression change patterns that were identified globally may represent novel opportunities for better control of RA through early diagnosis and development of alternative therapeutic strategies.

Publication Title

No associated publication

Alternate Accession IDs

E-GEOD-7657

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon GSE14242
Novel Regulators of Fgf23 Expression and Mineralization in Hyp Bone
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon

Description

We used gene array analysis of cortical bone to identify Phex-dependent gene transcripts regulating Fgf23 production and mineralization in Hyp mice. We discovered that activation of Fgf receptor- and Wnt-pathways contribute to increased Ffg23 gene transcription in Hyp bone. We found evidence in Hyp bone for increased expression of Fgf1, Fgf7, and Egr2 in the Fgf-signaling pathway and decrements in Sost and Cpz and increments in Sfrp1 and 4 in the Wnt-signaling pathway. Moreover, activation of Fgf and Wnt-signaling stimulated, whereas Tgf inhibited Fgf23 promoter activity in osteoblasts. We also observed reductions in Bmp1, a metalloproteinase that metabolizes the Fgf23 regulatory extracellular matrix protein Dmp1. These findings suggest that elevation of Fgf23 expression in osteocytes is regulated by interactions between cell surface expression of Phex, extracellular matrix proteins and paracrine effects of Fgf and Wnt. Alterations were also found in enzymes regulating the posttranslational processing and stability of Fgf23, including decrements in the glycosyltransferase Galnt3 and the proprotein convertase Pcsk5. In addition, we found that the Pcsk5 and the glycosyltransferase Galnt3 were decreased in Hyp bone, suggesting that reduced post-translational processing of FGF23 may also contribute to increased Fgf23 levels in Hyp mice. With regards to mineralization, we identified additional candidates to explain the intrinsic mineralization defect in Hyp osteoblasts, including increases in the mineralization inhibitors Mgp and Thbs4, as well as increases in local pH altering factors, carbonic anhydrase 12 (Car12) and 3 (Car3) and the sodium-dependent citrate transporter (Slc13a5). These studies demonstrate the complexity of gene expression alterations in bone that accompanies inactivating Phex mutations and identify novel pathways that may coordinate Fgf23 expression and mineralization of extracellular matrix in Hyp bone.

Publication Title

Novel regulators of Fgf23 expression and mineralization in Hyp bone.

Alternate Accession IDs

E-GEOD-14242

Sample Metadata Fields

Sex, Age, Specimen part

View Samples
accession-icon GSE40540
IP of 5-hydroxymethylcytosine (5-hmC) and 5-methylcytosine (5-mC) enriched DNA fragments from control and PB treated mouse livers
  • organism-icon Mus musculus
  • sample-icon 10 Downloadable Samples
  • Technology Badge Icon

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Dynamic changes in 5-hydroxymethylation signatures underpin early and late events in drug exposed liver.

Alternate Accession IDs

E-GEOD-40540

Sample Metadata Fields

Sex, Specimen part, Treatment, Time

View Samples
accession-icon GSE9444
Sleep deprivation and the brain
  • organism-icon Mus musculus
  • sample-icon 93 Downloadable Samples
  • Technology Badge Icon

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Homer1a is a core brain molecular correlate of sleep loss.

Alternate Accession IDs

E-GEOD-9444

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon GSE16387
Licensing of PPARg-regulated gene expression by IL-4-induced alternative macrophage activation
  • organism-icon Mus musculus, Homo sapiens
  • sample-icon 2 Downloadable Samples
  • Technology Badge Icon

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

STAT6 transcription factor is a facilitator of the nuclear receptor PPARγ-regulated gene expression in macrophages and dendritic cells.

Alternate Accession IDs

E-GEOD-16387

Sample Metadata Fields

Specimen part, Treatment, Subject, Time

View Samples
accession-icon GSE10026
High resolution gene expression profiling for simultaneous analysis of RNA synthesis, abundance and decay
  • organism-icon Mus musculus, Homo sapiens
  • sample-icon 36 Downloadable Samples
  • Technology Badge Icon

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Conserved principles of mammalian transcriptional regulation revealed by RNA half-life.

Alternate Accession IDs

E-GEOD-10026

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon GSE10744
Copy number variation and gene expression in the mouse
  • organism-icon Mus musculus
  • sample-icon 108 Downloadable Samples
  • Technology Badge Icon

Description

Copy number variation (CNV) of DNA segments has recently been identified as a major source of genetic diversity, but a more comprehensive understanding of the extent and phenotypic effect of this type of variation is only beginning to emerge. In this study we generated genome-wide expression data from 6 mouse tissues to investigate how CNVs influence gene expression.

Publication Title

Segmental copy number variation shapes tissue transcriptomes.

Alternate Accession IDs

E-GEOD-10744

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon GSE17667
Pou5f1 transcription targets in zebrafish
  • organism-icon Danio rerio
  • sample-icon 3 Downloadable Samples
  • Technology Badge Icon

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Zebrafish Pou5f1-dependent transcriptional networks in temporal control of early development.

Alternate Accession IDs

E-GEOD-17667

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon GSE26600
Cycad Genotoxin Methylazoxymethanol (MAM) Modulates Cellular Pathways Involved in Cancer and Neurodegenerative Disease
  • organism-icon Mus musculus
  • sample-icon 91 Downloadable Samples
  • Technology Badge Icon

Description

Methylazoxymethanol (MAM), the genotoxic metabolite of the cycad azoxyglucoside cycasin, induces genetic alterations in bacteria, yeast, plants, insects and mammalian cells, but adult nerve cells are thought to be unaffected. We show that the brains of young adult mice treated with a single systemic dose of MAM display DNA damage (O6-methylguanine lesions) that peaks at 48 hours and decline to near-normal levels at 7 days post-treatment. By contrast, at this time, MAM-treated mice lacking the gene encoding the DNA repair enzyme O6-methylguanine DNA methyltransferase (MGMT), showed persistent O6-methylguanine DNA damage. The DNA damage was linked to cell-signaling pathways that are perturbed in cancer and neurodegenerative disease. These data are consistent with the established carcinogenic and developmental neurotoxic properties of MAM in rodents, and they support the proposal that cancer and neurodegeneration share common signal transduction pathways. They also strengthen the hypothesis that early life exposure to the MAM glucoside cycasin has an etiological association with a declining, prototypical neurodegenerative disease seen in Guam, Japan, and New Guinea populations that formerly used the neurotoxic cycad plant for medicine and/or food. Exposure to environmental genotoxins may have relevance to the etiology of related tauopathies, notably, Alzheimers disease, as well as cancer.

Publication Title

The cycad genotoxin MAM modulates brain cellular pathways involved in neurodegenerative disease and cancer in a DNA damage-linked manner.

Alternate Accession IDs

E-GEOD-26600

Sample Metadata Fields

Sex, Specimen part, Time

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
Version 1.42.67-hotfix - .0.0