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accession-icon GSE15610
Knockout of the selenocysteine tRNA (Trsp) gene in mouse macrophage
  • organism-icon Mus musculus
  • sample-icon 10 Downloadable Samples
  • Technology Badge Icon

Description

Comparative analysis of gene expression in bone marrow-derived macrophages (BMDM) from trsp knockout mice (Trspfl/fl-LysM-Cre+/-) and Control (Trspfl/fl-LysM-Cre-/-) mice.

Publication Title

Selenoproteins regulate macrophage invasiveness and extracellular matrix-related gene expression.

Sample Metadata Fields

Sex, Treatment

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accession-icon GSE74677
Examination of loss of Selenophosphate Synthetase 1 (SPS1) in mouse tissues and cells
  • organism-icon Mus musculus
  • sample-icon 8 Downloadable Samples
  • Technology Badge Icon

Description

To examine the role of SPS1 in mammals, we generated a Sps1 knockout mouse and found that systemic SPS1 deficiency was embryonic lethal. Embryos were clearly underdeveloped by E8.5 and virtually reabsorbed by E14.5. Removal of Sps1 specifically in hepatocytes using Albumin-cre preserved viability, but significantly affected expression of a large number of mRNAs involved in cancer, embryonic development and the glutathione system. Particularly notable was the extreme deficiency of glutaredoxin 1 (GLRX1) and glutathione-S-transferase omega 1. To assess these phenotypes at the cellular level, we targeted the removal of SPS1 in F9 cells, a mouse embryonal carcinoma cell line, which recapitulated changes in the glutathione system proteins. We further found that several malignant characteristics of SPS1-deficient F9 cells were reversed, suggesting that SPS1 has a role in supporting and/or sustaining cancer. In addition, the increased ROS levels observed in F9 SPS1/GLRX1 deficient cells were reversed and became more like those in F9 SPS1 sufficient cells by overexpressing mouse or human GLRX1. The results suggest that SPS1 is an essential mammalian enzyme with roles in regulating redox homeostasis and controlling cell growth.

Publication Title

Selenophosphate synthetase 1 is an essential protein with roles in regulation of redox homoeostasis in mammals.

Sample Metadata Fields

Sex, Specimen part

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accession-icon GSE21583
Effects of ACE2 on BMPR2 mutation-mediated defects in gene expression
  • organism-icon Mus musculus
  • sample-icon 8 Downloadable Samples
  • Technology Badge Icon

Description

BMPR2 mutation causes pulmonary arterial hypertension (PAH); ACE2 treatment can resolve established BMPR2-mediated PAH. The purpose of this study was to uncover the molecular mechanism behind this.

Publication Title

Cytoskeletal defects in Bmpr2-associated pulmonary arterial hypertension.

Sample Metadata Fields

Sex, Specimen part, Treatment

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accession-icon GSE48383
ChIp-Chip using RNAP II, CREB C/EBPb and cJun antibody in undifferentiated or differentiated keratinocytes
  • organism-icon Mus musculus
  • sample-icon 10 Downloadable Samples
  • Technology Badge Icon

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Combinatorial recruitment of CREB, C/EBPβ and c-Jun determines activation of promoters upon keratinocyte differentiation.

Sample Metadata Fields

Specimen part, Treatment

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accession-icon GSE27302
Expression data from mouse colon tissue response to T cell transfer at week 0, 2, 4 and 6
  • organism-icon Mus musculus
  • sample-icon 16 Downloadable Samples
  • Technology Badge Icon

Description

Temporal geneome profiling of T cell transfer colitis model

Publication Title

Temporal genome expression profile analysis during t-cell-mediated colitis: identification of novel targets and pathways.

Sample Metadata Fields

Specimen part, Treatment, Time

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accession-icon GSE48382
ChIp-Chip using RNAP II, CREB C/EBPb and cJun antibody in undifferentiated or differentiated keratinocytes (expression)
  • organism-icon Mus musculus
  • sample-icon 10 Downloadable Samples
  • Technology Badge Icon

Description

Combinatorial recruitment of CREB, C/EBPb and Jun determines activation of promoters upon keratinocyte differentiation

Publication Title

Combinatorial recruitment of CREB, C/EBPβ and c-Jun determines activation of promoters upon keratinocyte differentiation.

Sample Metadata Fields

Specimen part, Treatment

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accession-icon GSE19320
Zebrafish early eye development
  • organism-icon Danio rerio
  • sample-icon 1 Downloadable Sample
  • Technology Badge Icon

Description

Gene expression profiling of zebrafish early eye development on 3 to 5 days post fertilization (dpf)

Publication Title

Integrating multiple genome annotation databases improves the interpretation of microarray gene expression data.

Sample Metadata Fields

Specimen part

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accession-icon GSE68842
A Long Non-coding RNA, LncMyoD, Regulates Skeletal Muscle Differentiation by Blocking IMP2-mediated mRNA Translation
  • organism-icon Mus musculus
  • sample-icon 1 Downloadable Sample
  • Technology Badge Icon

Description

Increasing evidence suggests that Long non-coding RNAs (LncRNAs) represent a new class of regulators of stem cells. However, the roles of LncRNAs in stem cell maintenance and myogenesis remain largely unexamined. For this study, hundreds of novel intergenic LncRNAs were identified that are expressed in myoblasts and regulated during differentiation. One of these LncRNAs, termed LncMyoD, is encoded next to the Myod gene and is directly activated by MyoD during myoblast differentiation. Knockdown of LncMyoD strongly inhibits terminal muscle differentiation largely due to a failure to exit the cell cycle. LncMyoD directly binds to IGF2-mRNA-binding-protein 2 (IMP2) and negatively regulates IMP2-mediated translation of proliferation genes such as N-Ras and c-Myc. While the RNA sequence of LncMyoD is not well-conserved between human and mouse, its locus, gene structure and function is preserved. The MyoD-LncMyoD-IMP2 pathway elucidates a mechanism as to how MyoD blocks proliferation to create a permissive state for differentiation.

Publication Title

A long non-coding RNA, LncMyoD, regulates skeletal muscle differentiation by blocking IMP2-mediated mRNA translation.

Sample Metadata Fields

Age

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accession-icon GSE27083
Expression data from MMTV-PDK1 transgenic mice
  • organism-icon Mus musculus
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon

Description

The role of PDK1 on mammary tumorigenesis and its interaction with PPARdelta, was assessed. Transgenic mice were generated in which PDK1 was expressed in the mammary epithelium.

Publication Title

PPARδ activation acts cooperatively with 3-phosphoinositide-dependent protein kinase-1 to enhance mammary tumorigenesis.

Sample Metadata Fields

Specimen part, Treatment

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accession-icon GSE10246
GNF Mouse GeneAtlas V3
  • organism-icon Mus musculus
  • sample-icon 39 Downloadable Samples
  • Technology Badge Icon

Description

High-throughput gene expression profiling has become an important tool for investigating transcriptional activity in a variety of biological samples. To date, the vast majority of these experiments have focused on specific biological processes and perturbations. Here, we profiled gene expression from a diverse array of normal tissues, organs, and cell lines in mice. Keywords: multiple tissues

Publication Title

Expression analysis of G Protein-Coupled Receptors in mouse macrophages.

Sample Metadata Fields

No sample metadata fields

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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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