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accession-icon GSE16002
Molecular Events Initiating B Cell Fate Specification
  • organism-icon Mus musculus
  • sample-icon 9 Downloadable Samples
  • Technology Badge Icon

Description

Functional genomics comparison of EBFko, Pax5ko, and RAG2ko cell lines.

Publication Title

Hoxa9 regulates Flt3 in lymphohematopoietic progenitors.

Sample Metadata Fields

Cell line

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accession-icon GSE25244
Patterns of gene expression associated with temporal phases of S. aureus infection
  • organism-icon Mus musculus
  • sample-icon 7 Downloadable Samples
  • Technology Badge Icon

Description

To acquire more information regarding the local immune events during the different phases of S. aureus infection, gene profiling using microarray technology was used to identify host genes whose expression is substantively altered in the kidneys during the acute (T2) and persistent phase of infection (T28). Genes associated with the distinct transcript profiles were identified by comparing the relative abundance of transcripts at 2 days (acute) and 28 days (persistent) of infection to their abundance in the kidneys of uninfected control animals (CTL).

Publication Title

The dynamics of T cells during persistent Staphylococcus aureus infection: from antigen-reactivity to in vivo anergy.

Sample Metadata Fields

Specimen part

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accession-icon GSE18216
Non-targeted effects of low dose ionizing radiation act via TGF to promote mammary carcinogenesis
  • organism-icon Mus musculus
  • sample-icon 65 Downloadable Samples
  • Technology Badge Icon

Description

It is widely believed that the carcinogenic action of ionizing radiation is due to targeted DNA damage and resulting mutations, but there is also substantial evidence that non-targeted radiation effects alter epithelial phenotype and the stromal microenvironment. Activation of transforming growth factor 1 (TGF) is a non-targeted radiation effect that mediates cell fate decisions following DNA damage and regulates microenvironment composition; it could either suppress or promote cancer. We asked if such non-targeted radiation effects contribute to carcinogenesis by using a novel radiation chimera model. Unirradiated Trp53 null mammary epithelium was transplanted to the mammary stroma, previously divested of endogenous epithelia, of mice previously exposed to a single low (10 -100 cGy) radiation dose. By 300 days, 100% of transplants in irradiated hosts at either 10 or 100 cGy had developed Trp53 null breast carcinomas compared to 54% in unirradiated hosts. Tumor growth rate was also increased by high, but not low, dose host irradiation. In contrast, irradiation of Tgfb1 heterozygote mice prior to transplantation failed to decrease tumor latency, or increase growth rate at any dose. Host irradiation significantly reduced the latency of invasive ductal carcinoma compared to spindle cell carcinoma. However, irradiation of either host genotype significantly increased the frequency of estrogen receptor negative tumors. These data demonstrate two concepts critical to understanding radiation risks. First, non-targeted radiation effects can significantly promote the frequency and alter the features of epithelial cancer. Second, radiation-induced TGF activity is a key mechanism of tumor promotion.

Publication Title

Radiation acts on the microenvironment to affect breast carcinogenesis by distinct mechanisms that decrease cancer latency and affect tumor type.

Sample Metadata Fields

Age, Specimen part

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accession-icon GSE87557
Role of annexin A2 in muscle repair
  • organism-icon Mus musculus
  • sample-icon 7 Downloadable Samples
  • Technology Badge Icon

Description

Repair of injured muscle involves repair of injured myofibers through the involvement of dysferlin and its interacting partners, including annexin. Studies with mice and patients have established that dysferlin deficit leads to chronic inflammation and adipogenic replacement of the diseased muscle. However, longitudinal analysis of annexin deficit on muscle pathology and function is lacking. Here we show that unlike annexin A1, but similar to dysferlin, lack of annexin A2 (AnxA2) causes poor myofiber repair and progressive weakening with age. However, unlike dysferlin-deficient muscle, AnxA2-deficient muscles do not exhibit chronic inflammation or adipogenic replacement. Deletion of AnxA2 in dysferlin deficient mice reduces inflammation, adipogenic replacement, and loss in muscle function caused by dysferlin deficit. These results show that: a) AnxA2 facilitates myofiber repair, b) chronic inflammation and adipogenic replacement of dysferlinopathic muscle requires AnxA2, and c) inhibiting AnxA2-mediated inflammation is a novel therapeutic avenue for dysferlinopathy.

Publication Title

Annexin A2 links poor myofiber repair with inflammation and adipogenic replacement of the injured muscle.

Sample Metadata Fields

Age, Specimen part

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accession-icon SRP003472
RNA-Seq analysis in mutant zebrafish reveals role of U1C protein in alternative splicing regulation
  • organism-icon Danio rerio
  • sample-icon 2 Downloadable Samples
  • Technology Badge IconIlluminaGenomeAnalyzerII

Description

Precise 5' splice site recognition is essential for both constitutive and regulated pre-mRNA splicing. The U1 snRNP specific protein U1C is involved in this first step of spliceosome assembly and important for stabilizing early splicing complexes. We used an embryonically lethal U1C knockout mutant zebrafish, hi1371, to investigate the potential genomewide role of U1C for splicing regulation. Surprisingly, genomewide RNA-Seq analysis of mutant versus wildtype embryos revealed a large set of specific target genes that changed their alternative splicing patterns in the absence of U1C. In sum, our findings provide evidence for a new role of a general snRNP protein, U1C, as a mediator of alternative splicing regulation.

Publication Title

RNA-Seq analysis in mutant zebrafish reveals role of U1C protein in alternative splicing regulation.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE108208
Expression data from cells located at the invasive front and in the tumor mass of mouse cervical squamous cell carcinomas
  • organism-icon Mus musculus
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon

Description

Cells located at the invasive front and in the tumor mass of mouse cervical squamous cell carcinomas were isolated by laser microdissection from hematoxylin-stained HPV/E2 sections. 7 months old HPV/E2 mice treated with oestrogen develop invasive cervical squamous cell carcinomas. This model recapitulates human invasive cervical neoplasias.

Publication Title

Inflammatory Cytokines Induce Podoplanin Expression at the Tumor Invasive Front.

Sample Metadata Fields

Specimen part

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accession-icon GSE30012
A latent pro-survival function for the mir-290-295 cluster in mouse embryonic stem cells.
  • organism-icon Mus musculus
  • sample-icon 5 Downloadable Samples
  • Technology Badge Icon

Description

MicroRNAs (miRNAs) post-transcriptionally regulate the expression of thousands of distinct mRNAs. While some regulatory interactions help to maintain basal cellular functions, others are likely relevant in more specific settings, such as response to stress. Here we describe such a role for the mir-290-295 cluster, the dominant miRNA cluster in mouse embryonic stem cells (mESCs). Examination of a target list generated from bioinformatic prediction, as well as expression data following miRNA loss, revealed strong enrichment for apoptotic regulators, two of which we validated directly: Caspase 2, the most highly conserved mammalian caspase, and Ei24, a p53 transcriptional target. Consistent with these predictions, mESCs lacking miRNAs were more likely to initiate apoptosis following genotoxic exposure to gamma irradiation or doxorubicin. Knockdown of either candidate partially rescued this pro-apoptotic phenotype, as did transfection of members of the mir-290-295 cluster. These findings were recapitulated in a specific mir-290-295 deletion line, confirming that they reflect miRNA functions at physiological levels. In contrast to the basal regulatory roles previously identified, the pro-survival phenotype shown here may be most relevant to stressful gestations, where pro-oxidant metabolic states induce DNA damage. Similarly, this cluster may mediate chemotherapeutic resistance in a neoplastic context, making it a useful clinical target.

Publication Title

A latent pro-survival function for the mir-290-295 cluster in mouse embryonic stem cells.

Sample Metadata Fields

Specimen part

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accession-icon GSE51089
Expression data from E12.5 and E14.5 mouse embryonic gonad of wild type (WT) and Wnt-4 knock-out (KO) mice. [Mouse430_2]
  • organism-icon Mus musculus
  • sample-icon 16 Downloadable Samples
  • Technology Badge Icon

Description

Wnt-4 signaling is critical for embryonic female sexual development. When Wnt-4 gene is deleted during embryonic development, the knock-out females present a partial sex reversal.

Publication Title

Identification of the genes regulated by Wnt-4, a critical signal for commitment of the ovary.

Sample Metadata Fields

Specimen part

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accession-icon GSE33302
Expression data from sleep deprivation experiment in mouse hippocampus
  • organism-icon Mus musculus
  • sample-icon 17 Downloadable Samples
  • Technology Badge Icon

Description

We used microarrays to detail the global programme of gene expression underlying the effect of sleep deprivation in the mouse hippocampus and identified distinct classes of regulated genes during this process.

Publication Title

Genomic analysis of sleep deprivation reveals translational regulation in the hippocampus.

Sample Metadata Fields

Age, Specimen part, Treatment

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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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