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accession-icon GSE21154
Gene array data for Fas knock-out human cancer cell line and mouse liver tissue
  • organism-icon Mus musculus, Homo sapiens
  • sample-icon 7 Downloadable Samples
  • Technology Badge Icon

Description

CD95 (also called FAS and APO-1) is a prototypical death receptor that

Publication Title

CD95 promotes tumour growth.

Sample Metadata Fields

Sex, Age, Specimen part, Cell line

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accession-icon GSE6514
Gene expression in the mouse brain during spontaneous sleep and prolonged wakefulness
  • organism-icon Mus musculus
  • sample-icon 86 Downloadable Samples
  • Technology Badge Icon

Description

These studies address temporal changes in gene expression during spontaneous sleep and extended wakefulness in the mouse cerebral cortex, a neuronal target for processes that control sleep; and the hypothalamus, an important site of sleep regulatory processes. We determined these changes by comparing expression in sleeping animals sacrificed at different times during the lights on period, to that in animals sleep deprived and sacrificed at the same diurnal time.

Publication Title

Macromolecule biosynthesis: a key function of sleep.

Sample Metadata Fields

Sex, Age, Specimen part

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accession-icon GSE25639
A mouse model of deregulation of the malt1 oncogene recapitulates the pathogenesis of human malt lymphoma
  • organism-icon Mus musculus, Homo sapiens
  • sample-icon 10 Downloadable Samples
  • Technology Badge Icon

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Expression of MALT1 oncogene in hematopoietic stem/progenitor cells recapitulates the pathogenesis of human lymphoma in mice.

Sample Metadata Fields

Specimen part, Disease

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accession-icon GSE23725
Expression data from mouse neonatal ovarian xenobiotic culture experiments
  • organism-icon Mus musculus
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon

Description

Mammalian females are born with a finite number of non-renewing primordial follicles, the majority of which remain in a quiescent state for many years. Due to their non-renewing nature, these resting oocytes are particularly vulnerable to xenobiotic insult, resulting in premature ovarian senescence and the formation of dysfunctional oocytes. In this study we characterised the mechanisms of ovotoxicity for three ovotoxic agents, 4-Vinylcyclohexene Diepoxide (VCD), Methoxychlor (MXC), and Menadione (MEN), all of which target immature follicles. Neonatal mouse ovaries (PND3-4) were cultured in the presence of 4-Vinylcyclohexene Diepoxide (50uM), Methoxychlor (50uM), and Menadione (5uM) for 96 hours to observe their effects on the ovarian transcriptome. This was done in the hopes of gaining a better understanding of the mechanisms underpinning xenobiotic induced pre-antral ovotoxicity.

Publication Title

Adding insult to injury: effects of xenobiotic-induced preantral ovotoxicity on ovarian development and oocyte fusibility.

Sample Metadata Fields

Specimen part

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accession-icon GSE34568
The transcription factor CDX2 maintains active enhancer in intestinal villus cells in vivo
  • organism-icon Mus musculus
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Intestinal master transcription factor CDX2 controls chromatin access for partner transcription factor binding.

Sample Metadata Fields

Specimen part

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accession-icon GSE19836
A mouse Embryonic Stem Cell Bank for inducible overexpression of human chromosome 21 genes
  • organism-icon Mus musculus
  • sample-icon 32 Downloadable Samples
  • Technology Badge Icon

Description

The HSA21-mES Cell Bank includes, in triplicate clones, thirty-two murine orthologs of HSA21 genes, which can be overexpressed in an inducible manner using the Tet-off system integrated in the Rosa26 locus.

Publication Title

A mouse embryonic stem cell bank for inducible overexpression of human chromosome 21 genes.

Sample Metadata Fields

Specimen part

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accession-icon GSE52797
Expression data of Myh6-MeCP2 transgenic mice
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon

Description

Hearts of Myh6-MeCP2 transgenic mice and wildtype littermates were rapidly dissected and flash frozen.

Publication Title

Adrenergic Repression of the Epigenetic Reader MeCP2 Facilitates Cardiac Adaptation in Chronic Heart Failure.

Sample Metadata Fields

Specimen part

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accession-icon SRP346110
Anakinra restores cellular proteostasis by coupling mitochondrial redox balance to autophagy
  • organism-icon Mus musculus
  • sample-icon 4 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

Autophagy selectively degrades aggregation-prone misfolded proteins caused by defective cellular proteostasis. However, the complexity of autophagy may prevent the full appreciation of how its modulation could be used as a therapeutic strategy in disease management. Here we define a molecular pathway through which recombinant interleukin-1 receptor antagonist (IL-1Ra, anakinra) affects cellular proteostasis independently from the IL-1 receptor (IL-1R1). Anakinra promoted H2O2-driven autophagy through a xenobiotic sensing pathway involving the aryl hydrocarbon receptor that, activated through the indoleamine 2,3-dioxygenase 1-kynurenine pathway, transcriptionally activates NADPH Oxidase 4 independent of the IL-1R1. By coupling the mitochondrial redox balance to autophagy, anakinra improved the dysregulated proteostasis network in murine and human cystic fibrosis. We anticipate that anakinra may represent a therapeutic option in addition to its IL-1R1 dependent anti-inflammatory properties by acting at the intersection of mitochondrial oxidative stress and autophagy with the capacity to restore conditions in which defective proteostasis leads to human disease. Overall design: mRNA profiles of alveolar macrophages purified from C57BL/6 and Il1r1-/- mice treated or not with Anakinra

Publication Title

Anakinra restores cellular proteostasis by coupling mitochondrial redox balance to autophagy.

Sample Metadata Fields

Specimen part, Genotype, Subject

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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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