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accession-icon GSE16475
Expression data from side population subfraction hematopoietic stem cells
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon

Description

The traditional view of hematopoiesis has been that all the cells of the peripheral blood are the progeny of a unitary homogeneous pool of hematopoietic stem cells (HSCs). Recent evidence suggests that the hematopoietic system is actually maintained by a consortium of HSC subtypes with distinct functional characteristics. We show here that myeloid-biased HSCs (My-HSCs) and lymphoid-biased (Ly-HSCs) can be purified according to their capacity for Hoechst dye efflux in combination with canonical HSC markers.

Publication Title

Distinct hematopoietic stem cell subtypes are differentially regulated by TGF-beta1.

Sample Metadata Fields

Sex, Specimen part

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accession-icon GSE102444
Staphylococcus aureus evades macrophage killing through NLRP3 dependent effects on mitochondrial trafficking
  • organism-icon Mus musculus
  • sample-icon 9 Downloadable Samples
  • Technology Badge Icon

Description

Respiratory innate immunity requires alveolar macrophages, which are specifically targeted by the S. aureus toxin alpha toxin. These data compare the response of alveolar macrophages to S. aureus with or without alpha toxin neutralization.

Publication Title

S. aureus Evades Macrophage Killing through NLRP3-Dependent Effects on Mitochondrial Trafficking.

Sample Metadata Fields

Sex, Age, Specimen part, Treatment

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accession-icon GSE10467
Investigating genes regulated by mir-155 in a mouse macrophage cell line
  • organism-icon Mus musculus
  • sample-icon 2 Downloadable Samples
  • Technology Badge Icon

Description

Mammalian microRNAs (miRNAs) are emerging as key regulators of the development and function of the immune system. Here, we report a strong but transient induction of miR-155 in mouse bone marrow after injection of bacterial lipopolysaccharide (LPS) correlated with granulocyte/monocyte (GM) expansion. Demonstrating the sufficiency of miR-155 to drive GM expansion, enforced expression in mouse bone marrow cells caused GM proliferation in a manner reminiscent of LPS treatment. However, the mir-155-induced GM populations displayed pathological features characteristic of myeloid neoplasia. Extending possible relevance to human disease, miR-155 was overexpressed in the bone marrow of patients with acute myeloid leukemia (AML). Furthermore, miR-155 repressed a subset of genes implicated in hematopoietic development and disease. These data implicate miR-155 as a contributor to physiological GM expansion during inflammation and to certain pathological features associated with AML, emphasizing the importance of proper miR-155 regulation in developing myeloid cells during times of inflammatory stress.

Publication Title

Sustained expression of microRNA-155 in hematopoietic stem cells causes a myeloproliferative disorder.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE32422
Expression data from the dorsal and lateral lobes of the prostates of TRAMP mice treated with OSU-CG5
  • organism-icon Mus musculus
  • sample-icon 5 Downloadable Samples
  • Technology Badge Icon

Description

Cells undergoing malignant transformation often shift their cellular metabolism from primarily oxidative phosphorylation to aerobic glycolysis (the Warburg effect). Energy restriction-mimetic agents (ERMAs), such as 2-deoxyglucose and resveratrol, that target this shift in cellular metabolism have been effective in inhibiting cancer cell growth in vitro, and xenograft tumor growth in vivo.

Publication Title

Suppression of prostate epithelial proliferation and intraprostatic progrowth signaling in transgenic mice by a new energy restriction-mimetic agent.

Sample Metadata Fields

Specimen part

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accession-icon GSE35734
Screening of genes involved in chromosome segregation in meiosis I
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon

Description

Prophase I of meiosis involves dynamic chromosome segregation processes including synapsis, meiotic recombination, and cohesion. Genetic defects in genes participating in these processes consistently cause reproduction failure in mice. To identify candidate genes responsible for infertility or recurrent pregnancy loss in humans, we performed expression profiling of male and female gonads of mice undergoing meiotic prophase I.

Publication Title

Screening of genes involved in chromosome segregation during meiosis I: in vitro gene transfer to mouse fetal oocytes.

Sample Metadata Fields

Sex, Age, Specimen part

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accession-icon GSE101165
Expression data of wildtype and miR-146a-deficient 2D2 transgenic T cells
  • organism-icon Mus musculus
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon

Description

We used the Affymetrix GeneChip Mouse Genome 430 2.0 Arrays to compare the gene expression profiles of wildtype and miR-146a-deficient 2D2 transgenic T cells.

Publication Title

miR-146a modulates autoreactive Th17 cell differentiation and regulates organ-specific autoimmunity.

Sample Metadata Fields

Specimen part

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accession-icon GSE13730
BALB/c mice genetically susceptible to proteoglycan-induced arthritis and spondylitis
  • organism-icon Mus musculus
  • sample-icon 12 Downloadable Samples
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Description

BALB/c mice are susceptible to proteoglycan (PG) aggrecan-induced arthritis (PGIA), a murine model of rheumatoid arthritis (Glant,T.T. and Mikecz,K., Proteoglycan aggrecan-induced arthritis. A murine autoimmune model of rheumatoid arthritis. Methods Mol.Med. 2004. 102: 313-338.). However, there are marked differences among BALB/c colonies (maintained by different vendors at different locations) in PGIA onset and severity, which could be the result of subtle variations in their genetic background.

Publication Title

BALB/c mice genetically susceptible to proteoglycan-induced arthritis and spondylitis show colony-dependent differences in disease penetrance.

Sample Metadata Fields

Sex

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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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