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accession-icon GSE10658
IL-9/mast cell-mediated intestinal permeability predispose to oral antigen hypersensitivity
  • organism-icon Mus musculus
  • sample-icon 2 Downloadable Samples
  • Technology Badge Icon

Description

Small intestine of a pool of three Wt mice and a pool of 3 IL-9tg mice in a balb/c backround.

Publication Title

IL-9- and mast cell-mediated intestinal permeability predisposes to oral antigen hypersensitivity.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE63068
Integrative genomic signatures of hepatocellular carcinoma derived from nonalcoholic fatty liver disease
  • organism-icon Mus musculus, Homo sapiens
  • sample-icon 72 Downloadable Samples
  • Technology Badge Icon

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Integrative genomic signatures of hepatocellular carcinoma derived from nonalcoholic Fatty liver disease.

Sample Metadata Fields

Age, Specimen part, Disease

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accession-icon GSE63027
Expression data from GNMT and MAT1A knockout models that develop all the stages of non-alcoholic fatty liver disease including hepatocellular carcinoma [GNMT_MAT1A_3&8_months]
  • organism-icon Mus musculus
  • sample-icon 39 Downloadable Samples
  • Technology Badge Icon

Description

Liver global gene expression patterns of 9 GNMT-knockout mice histopathologically determined to have non-alcoholic steatohepatitis (NASH) and hepatocellular carcinoma (HCC) together with 10 MAT1A-knockout mice histopathologically determined to have steatosis and NASH. All these have their respective wild type patterns. These were analyzed to define signatures to study the pathogenesis of NAFLD-derived HCC, explore which subtypes of cancers can be investigated using mouse models and define a signature of HCC differential survival that can be used to characterize HCC subtypes of different survival derived from mixed etiologies.

Publication Title

Integrative genomic signatures of hepatocellular carcinoma derived from nonalcoholic Fatty liver disease.

Sample Metadata Fields

Age, Specimen part, Disease

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accession-icon GSE12908
Gene expression following miR-30a knockdown in bipotential mouse embryonic liver (BMEL) cells
  • organism-icon Mus musculus
  • sample-icon 10 Downloadable Samples
  • Technology Badge Icon

Description

The goal was to identify genes targeted by miR-30a.

Publication Title

The microRNA-30 family is required for vertebrate hepatobiliary development.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE10765
Expression data from MALP-2-stimulated macrophages from wild-type, IRAK-2-/- and IRAK-1-/IRAK-2-/- mice
  • organism-icon Mus musculus
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon

Description

IL-1R-associated kinases (IRAKs) participate in Toll-like receptor (TLR) signal transduction. MALP-2 is a TLR2 ligand, and stimulation of macrophages with MALP-2 activates expression of various genes including proinflammatory cytokines.

Publication Title

Sequential control of Toll-like receptor-dependent responses by IRAK1 and IRAK2.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE7487
Gene profiling of pathological cardiac hypertrophy vs physiological hypertrophy
  • organism-icon Mus musculus
  • sample-icon 23 Downloadable Samples
  • Technology Badge Icon

Description

Cardiac hypertrophy can lead to heart failure, and is induced either by physiological stimuli eg postnatal development, chronic exercise training or pathological stimuli eg pressure or volume overload. Majority of new therapies for heart failure has mixed outcomes. A combined mouse model and oligo-array approach are used to examine whether phosphoinositide 3-kinase (p110-alpha isoform) activity is critical for maintenance of cardiac function and long-term survival in a setting of heart failure. The significance and expected outcome are to recognise genes involved in models of heart failure ie pathological- vs physiology-hypertrophy, and examine the molecular mechanisms responsible for such activity.

Publication Title

PI3K(p110 alpha) protects against myocardial infarction-induced heart failure: identification of PI3K-regulated miRNA and mRNA.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE23306
The JMJD3-IRF4 axis regulates M2 macrophage polarization and host responses against helminth infection
  • organism-icon Mus musculus
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon

Description

Polarization of macrophages to M1 or M2 cells is important for mounting responses against bacterial and helminth infection respectively. Jumonji domain containing 3 (JMJD3), a histone 3 K27 demethylase, has been implicated in the activation of macrophages. Here we show that JMJD3 is essential for M2 macrophage polarization to helminth infection and chitin, though JMJD3 is dispensable for M1 responses. Furthermore, Jmjd3 is critical for proper bone marrow macrophage differentiation in a demethylase activity-dependent manner. Jmjd3 deficiency affected trimethylation of H3K27 in only a limited numbers of genes. Among them, we identified Irf4 as the target transcription factor critical for controlling M2 macrophage polarization. Collectively, these results show that JMJD3-mediated H3K27 demethylation is critical for regulating M2 macrophage development leading to anti-helminth host responses.

Publication Title

The Jmjd3-Irf4 axis regulates M2 macrophage polarization and host responses against helminth infection.

Sample Metadata Fields

Specimen part, Treatment

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accession-icon GSE27451
Functions of HDAC1 and HDAC2 in Schwann cells during postnatal
  • organism-icon Mus musculus
  • sample-icon 5 Downloadable Samples
  • Technology Badge Icon

Description

The aim of our study is to determine the functions of histone deacetylases (HDACs) 1 and 2 in Schwann cells during postnatal development of the peripheral nervous system (PNS). Schwann cells are the myelinating glial cells of the PNS. At birth, mouse sciatic nerves mature in 2 subsequent phases: 1/ big caliber axons get sorted into a 1 to 1 relationship with Schwann cells, 2/ Schwann cells build a myelin sheath around sorted axons. In mice where both HDAC1 & HDAC2 have been specifically knocked out in Schwann cells, both phases are impaired. HDACs are chromatin remodeling enzymes, they can thus alter gene expression directly. We want to identify which genes controlled by HDAC1 and HDAC2 in Schwann cells are necessary for the maturation of sciatic nerves. Because HDAC1 and HDAC2 can compensate for each other loss to some extend, we will first analyze changes of gene expression in HDAC1/HDAC2 double KO animals. We expect to gain critical insights into the molecular mechanisms controlling Schwann cell differentiation and myelination. This knowledge is of key importance for the success of regenerative medicine in peripheral neuropathies, nerve tumors, and transplantation paradigms in non-regenerative CNS lesions and in large PNS injuries.

Publication Title

HDAC1 and HDAC2 control the transcriptional program of myelination and the survival of Schwann cells.

Sample Metadata Fields

Disease, Disease stage

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accession-icon GSE62173
Expression data of mice cochlea treated with L-methionine and valproic acid.
  • organism-icon Mus musculus
  • sample-icon 16 Downloadable Samples
  • Technology Badge Icon

Description

Treatment of DBA/2J mice with a combination of L-methionine and valproic acid significantly attenuated progressive hearing loss. We examined gene expression in the whole cochlea of the mice. This study was aimed to detect genes of which change in expression levels were associated with attenuation of progressive hearing loss in the mice.

Publication Title

Attenuation of progressive hearing loss in DBA/2J mice by reagents that affect epigenetic modifications is associated with up-regulation of the zinc importer Zip4.

Sample Metadata Fields

Sex, Age, Specimen part

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accession-icon GSE53826
Expression data from bone marrow (BM) neutrophils
  • organism-icon Mus musculus
  • sample-icon 2 Downloadable Samples
  • Technology Badge Icon

Description

We employed GeneChip analysis to investigate the global gene expression profiles of neutrophils from BM

Publication Title

Neutrophil priming occurs in a sequential manner and can be visualized in living animals by monitoring IL-1β promoter activation.

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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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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