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accession-icon GSE134178
TNF deficiency causes changes in the spatial organization of neurogenic zones and the number of microglia and neurons in the cerebral cortex
  • organism-icon Mus musculus
  • sample-icon 8 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

Background: Although TNF inhibitors are used to treat chronic inflammatory diseases, there is little information about how long-term inhibition of TNF affects the homeostatic functions that TNF maintains in the intact CNS. TNF is known to modulate neurogenesis by decreasing cell proliferation, increasing apoptosis of precursor cells, and impairing neuronal differentiation. TNF can also influence the formation of the hippocampus, with long-lasting effects on cognition. Materials and methods: To clarify whether developmental TNF deficiency causes alterations in the naïve CNS, we estimated the number of proliferating cells, microglia, and neurons in the brains of E13.5, P7, and adult TNF +/+ and TNF-/- mice and measured changes in gene and protein expression and monoamine levels in adult TNF+/+ and TNF-/- mice. To evaluate long-term effects of TNF inhibitors, we treated healthy adult C57BL/6 mice with either saline, selective soluble TNF inhibitor XPro1595, or nonselective TNF inhibitor etanercept. We estimated changes in cell number and protein expression after two months of treatment. We assessed the effects of TNF deficiency on cognition by testing adult TNF+/+ and TNF-/- mice and anti-TNF treated mice with behavioral tasks.

Publication Title

TNF deficiency causes alterations in the spatial organization of neurogenic zones and alters the number of microglia and neurons in the cerebral cortex.

Sample Metadata Fields

Sex, Specimen part

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accession-icon GSE49326
Gene expression in Drosophila hemocytes at the onset of metamorphosis, and dependence to the Ecdysone Receptor
  • organism-icon Drosophila melanogaster
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Drosophila Gene 1.1 ST Array (drogene11st)

Description

Coupling immunity and development is essential to ensure survival despite changing internal conditions in the organism. The metamorphosis of the fruit fly represents a striking example of drastic and systemic physiological changes that need to be integrated with the innate immune system. However, the mechanisms that coordinate development and immune cell activity in the transition from larva to adult in Drosophila remain to elucidate. The steroid hormone ecdysone is known to act as a key coordinator of metamorphosis. This hormone activates a nuclear receptor, the Ecdysone Receptor (EcR), which acts as a heterodimer with its partner Ultraspiracle (USP). Together, they activate the transcription of primary response genes, which in turn activate the transcription of a battery of late response genes. We have revealed that regulation of macrophage-like cells (hemocytes) by the steroid hormone ecdysone is essential for an effective innate immune response over metamorphosis. We have shown that in response to ecdysone signalling, hemocytes rapidly up regulate actin dynamics, motility and phagocytosis of apoptotic corpses, and acquire the ability to chemotax to damaged epithelia. Most importantly, individuals lacking ecdysone-activated hemocytes are defective in bacterial phagocytosis and are fatally susceptible to infection by bacteria ingested at larval stages, despite the normal systemic production of antimicrobial peptides. This decrease in survival is comparable to the one observed in pupae lacking immune cells altogether, indicating that ecdysone-regulation is essential to hemocyte immune functions and survival after infection.

Publication Title

Steroid hormone signaling is essential to regulate innate immune cells and fight bacterial infection in Drosophila.

Sample Metadata Fields

Specimen part

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accession-icon GSE58509
BolA is a transcriptional switch that turns off motility and turns on biofilm development
  • organism-icon Escherichia coli str. k-12 substr. mg1655
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix E. coli Genome 2.0 Array (ecoli2)

Description

Bacteria are extremely versatile organisms which rapidly adapt to changing environments. When Escherichia coli cells switch from planktonic growth to biofilm, flagellum formation is turned off, and the production of fimbriae and extracellular polysaccharides is switched on. Here we show that BolA protein is a new bacterial transcription factor which modulates the switch from planktonic to sessile lifestyle. BolA negatively modulates flagella biosynthesis and thus swimming capacity. Furthermore, BolA overexpression favors biofilm formation and involvesinvolving fimbriae-like adhesins and curli production. Our results unraveled for the first time that BolA is a protein with high affinity to DNA, involved in the regulation of several genes of E. coli at a genome-wide scale level. Moreover, this observation further demonstrated that the most significant targets of this protein involved a complex network of genes encoding proteins extremely necessary in biofilm development processes. Herein we propose that BolA is a motile/adhesive transcriptional switch, specifically involved in the transition between the planktonic and the attachment stage of biofilm formation process.

Publication Title

BolA is a transcriptional switch that turns off motility and turns on biofilm development.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE71637
TCR signal strength controls thymic differentiation of discrete proinflammatory T cell subsetsistinct TCR signal strength requirements in the thymus
  • organism-icon Mus musculus
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 2.1 ST Array (mogene21st)

Description

The murine thymus produces discrete T cell subsets making either IFN- or IL-17, but the role of the TCR in this developmental process remains controversial. Here we generated a non-transgenic and polyclonal model of reduced TCR expression and signal strength selectively on T cells. Mice haploinsufficient for both CD3 and CD3 (CD3DH) showed normal thymocyte subsets but specific defects in T cell development, namely impaired differentiation of IL-17-producing embryonic V6+ (but not adult V4+) T cells and a marked depletion of IFN--producing CD122+ NK1.1+ (V1-biased) T cells throughout life. As result, adult CD3DH mice showed defective peripheral IFN- responses and were resistant to experimental cerebral malaria. Thus, strong TCR signaling is required within specific developmental windows with distinct V usage and differential cytokine production by effector T cell subsets.

Publication Title

TCR signal strength controls thymic differentiation of discrete proinflammatory γδ T cell subsets.

Sample Metadata Fields

Specimen part

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accession-icon GSE24427
Expression data of multiple sclerosis patients receiving subcutaneous Interferon-beta-1b therapy [U133 A and B]
  • organism-icon Homo sapiens
  • sample-icon 250 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A Array (hgu133a)

Description

The purpose of this study was to characterize the transcriptional effects induced by subcutaneous IFN-beta-1b treatment (Betaferon, 250 g every other day) in patients with relapsing-remitting form of multiple sclerosis (MS).

Publication Title

Long-term genome-wide blood RNA expression profiles yield novel molecular response candidates for IFN-beta-1b treatment in relapsing remitting MS.

Sample Metadata Fields

Sex

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accession-icon GSE86034
MicroRNA miR-92a-2 targets TFPI2 to ameliorate oxidative stress of the hypoxia neuron
  • organism-icon Rattus norvegicus
  • sample-icon 1 Downloadable Sample
  • Technology Badge IconIllumina ratRef-12 v1.0 expression beadchip

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

No associated publication

Sample Metadata Fields

Specimen part

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accession-icon GSE45516
Expression data from human Huntington fibroblasts
  • organism-icon Homo sapiens
  • sample-icon 9 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Gene expression profile comparison from fibroblasts of Huntington individuals and normal ones

Publication Title

Gene expression profile in fibroblasts of Huntington's disease patients and controls.

Sample Metadata Fields

Sex, Age, Specimen part, Disease

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accession-icon GSE85825
MicroRNA miR-92a-2 targets TFPI2 to ameliorate oxidative stress of the hypoxia neuron [mRNA]
  • organism-icon Rattus norvegicus
  • sample-icon 1 Downloadable Sample
  • Technology Badge IconIllumina ratRef-12 v1.0 expression beadchip

Description

Comparison of the differential expression mRNA profiles from the brain cortex of hypoxia and normaixa rats by silica microarray chip

Publication Title

No associated publication

Sample Metadata Fields

Specimen part

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accession-icon GSE12066
Segregation of genes influencing skeletal phenotypes in congenic P/NP rats
  • organism-icon Rattus norvegicus
  • sample-icon 20 Downloadable Samples
  • Technology Badge Icon Affymetrix Rat Genome 230 2.0 Array (rat2302)

Description

Bone mineral density and structure candidate gene analysis in alcohol-non-preferring (NP), alcohol-preferring (P), congenic NP (NP.P) and congenic P (P.NP) rats

Publication Title

Identification of genes influencing skeletal phenotypes in congenic P/NP rats.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE11180
Genomic expression analysis of rat chromosome 4 for skeletal traits at femoral neck
  • organism-icon Rattus norvegicus
  • sample-icon 16 Downloadable Samples
  • Technology Badge Icon Affymetrix Rat Genome 230 2.0 Array (rat2302)

Description

Femoral neck bone mineral density and structure candidate gene analysis in Fischer 344 (F344) and Lewis (LEW) rats

Publication Title

Genomic expression analysis of rat chromosome 4 for skeletal traits at femoral neck.

Sample Metadata Fields

No sample metadata fields

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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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