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accession-icon GSE11224
Expression data from developing mouse placenta
  • organism-icon Mus musculus
  • sample-icon 54 Downloadable Samples
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Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Genomic evolution of the placenta using co-option and duplication and divergence.

Sample Metadata Fields

Specimen part

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accession-icon GSE11220
Timecourse of developing mouse placenta, with placental and decidual tissues profiled separately
  • organism-icon Mus musculus
  • sample-icon 44 Downloadable Samples
  • Technology Badge Icon

Description

We used full genome microarrays to profile the full lifetime of the mouse placenta from embryonic day 8.5 (e8.5), at the time of chorioallantoic fusion, until postnatal day 0 (P0).

Publication Title

Genomic evolution of the placenta using co-option and duplication and divergence.

Sample Metadata Fields

Specimen part

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accession-icon GSE11222
Placental and decidual timecourse samples normalized and modeled with an undissected e17 sample
  • organism-icon Mus musculus
  • sample-icon 8 Downloadable Samples
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Description

We used full genome microarrays to profile the full lifetime of the mouse placenta from embryonic day 8.5 (e8.5), at the time of chorioallantoic fusion, until postnatal day 0 (P0). For these samples, at each stage the fetal placenta and maternal decidual tissues were dissected and profiled separately (See series 1).

Publication Title

Genomic evolution of the placenta using co-option and duplication and divergence.

Sample Metadata Fields

Specimen part

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accession-icon GSE20152
The role of SphK1 in hTNF induced inflammation
  • organism-icon Mus musculus
  • sample-icon 3 Downloadable Samples
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Description

The study analyzes analyzes gene expression changes in the ankle joint in mouse TNFa overexpression models with or without sphingosine kinase 1 activity.

Publication Title

Genetic sphingosine kinase 1 deficiency significantly decreases synovial inflammation and joint erosions in murine TNF-alpha-induced arthritis.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE23738
Global changes of expression patterns of vaccinia virus infected lungs of C57BL/6 mice.
  • organism-icon Mus musculus
  • sample-icon 5 Downloadable Samples
  • Technology Badge Icon

Description

Vaccinia virus infection of mouse lungs produces a focal infection within the lung remaining at the large bronchi throughout the course of infection. Animals die of respiratory failure with little edema and few infiltrating immune cells. It is well established that poxviruses control the host immune system by encoding multiple host defense pathway antagonists.

Publication Title

Roles of vaccinia virus genes E3L and K3L and host genes PKR and RNase L during intratracheal infection of C57BL/6 mice.

Sample Metadata Fields

Specimen part

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accession-icon GSE23114
Cell cyclin kinase inhibitor Cdkn2c regulates B cell homeostasis and function in the NZM2410-derived murine lupus susceptibility locus Sle2c1
  • organism-icon Mus musculus
  • sample-icon 16 Downloadable Samples
  • Technology Badge Icon

Description

Sle2c1 is an NZM2410-derived lupus susceptibility locus that induces an expansion of the B1a cell compartment. B1a cells have a repertoire enriched for autoreactivity, and an expansion of this B cell subset occurs in several mouse models of lupus. Here we showed that expression of Sle2c1 enhances NZB cellular phenotypes that have been associated with autoimmune pathogenesis. A combination of genetic mapping and candidate gene analysis presents Cdkn2c, a gene encoding for cyclin kinase inhibitor p18INK4c (p18), as the top candidate gene for inducing the Slec2c1 associated expansion of B1a cells. A novel SNP in the Cdkn2c promoter is associated with a significantly reduced Cdkn2c expression in the splenic B cells and B1a cells from Sle2c1-carrying mice, which leads to defective G1 cell cycle arrest in splenic B cells and increased proliferation of Pc B1a cells. As cell cycle is differentially regulated in B1a and B2 cells, these results suggest that Cdkn2c play a critical role in B1a cell self renewal, and that its impaired expression leads to an accumulation of these cells with high autoreactive potential.

Publication Title

Cyclin-dependent kinase inhibitor Cdkn2c regulates B cell homeostasis and function in the NZM2410-derived murine lupus susceptibility locus Sle2c1.

Sample Metadata Fields

Specimen part

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accession-icon GSE22927
Hierarchical synergy of Pten, p53 and Rb pathways in high-grade astrocytoma induced in adult brain
  • organism-icon Mus musculus, Homo sapiens
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon

Description

Mutations in the PTEN, TP53 and RB1 pathways are obligate events in the pathogenesis of human glioblastomas, the highest grade of astrocytoma. To investigate synergy between these tumor suppressors in mice, we induced various combinations of compound deletions conditionally in astrocytes and neural precursors in the mature brain. The resulting highly penetrant astrocytomas showed a spectrum of histopathological variation reminiscent of human tumors, and ranged from grade III to grade IV (glioblastoma). Secondary somatic mutations varied depending on the combination of initiating deletions and were relevant to human disease. Receptor tyrosine kinase amplifications were frequent in tumors initiated by combined conditional deletion of Pten and Tp53, but not when Rb, Pten and Tp53 were simultaneously deleted. Multiple mutations within PI3K and Rb pathways were acquired, however, Mapk activation was not consistently detected in astrocytomas. Gene expression profiling revealed striking similarities to previously described human astrocytoma subclasses. A subset of astrocytomas initiated outside of proliferative niches in the adult brain.

Publication Title

Cooperativity within and among Pten, p53, and Rb pathways induces high-grade astrocytoma in adult brain.

Sample Metadata Fields

Sex, Specimen part

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accession-icon GSE25486
Nanoemulsion-Specific Gene Expression Data in Bone Marrow Derived Dendritic Cells and in Murine Nasal Epithelium
  • organism-icon Mus musculus
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Nanoemulsion mucosal adjuvant uniquely activates cytokine production by nasal ciliated epithelium and induces dendritic cell trafficking.

Sample Metadata Fields

Sex, Age, Specimen part, Time

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accession-icon GSE25485
Gene expression data in Bone Marrow Derived Dendritic Cells (BMDC) following nanoemulsion adjuvant exposure
  • organism-icon Mus musculus
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon

Description

Antigen uptake, processing and presentation by dendritic cells are regulated by complex intra- and inter-cellular signalling events. Typical vaccine adjuvants lead to the transcription of pro-inflammatory cytokines and chemokines which relate to immune induction.

Publication Title

Nanoemulsion mucosal adjuvant uniquely activates cytokine production by nasal ciliated epithelium and induces dendritic cell trafficking.

Sample Metadata Fields

Sex, Age, Specimen part, Time

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accession-icon GSE27429
Expression data at 24 hours after the blocking of Shh signaling in tooth germs at embryonic day 14
  • organism-icon Mus musculus
  • sample-icon 8 Downloadable Samples
  • Technology Badge Icon

Description

The genetic mechanism governing the spatial patterning of teeth still remains to be elucidated. Sonic hedgehog (Shh) is one of key signaling molecules involved in the spatial patterning of teeth. By utilizing maternal transfer of 5E1 (an IgG1 monoclonal antibody against Shh protein) through the placenta to block Shh signaling, we investigated the changes in tooth patterning and in gene expression.

Publication Title

Interactions between Shh, Sostdc1 and Wnt signaling and a new feedback loop for spatial patterning of the teeth.

Sample Metadata Fields

Specimen part, Time

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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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