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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 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

View Samples
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 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 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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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.

Sample Metadata Fields

Sex, Treatment

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accession-icon GSE30859
Multilineage Priming of Enhancer Repertoires Precedes Commitment to the B and Myeloid Cell Lineages in Hematopoietic Progenitors
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon

Description

Recent studies have documented genome-wide binding patterns of transcriptional regulators and their associated epigenetic marks in hematopoietic cell lineages. In order to determine how epigenetic marks are established and maintained during developmental progression, we have generated long-term cultures of hematopoietic progenitors by enforcing the expression of the E-protein antagonist Id2. Hematopoietic progenitors that express Id2 are multipotent and readily differentiate upon withdrawal of Id2 expression into committed B lineage cells, thus indicating a causative role for E2A (Tcf3) in promoting the B cell fate. Genome-wide analyses revealed that a substantial fraction of lymphoid and myeloid enhancers are premarked by the poised or active enhancer mark H3K4me1 in multipotent progenitors. Thus, in hematopoietic progenitors, multilineage priming of enhancer elements precedes commitment to the lymphoid or myeloid cell lineages.

Publication Title

Multilineage priming of enhancer repertoires precedes commitment to the B and myeloid cell lineages in hematopoietic progenitors.

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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