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accession-icon SRP150217
Widespread inter-individual gene expression variability in Arabidopsis thaliana
  • organism-icon Arabidopsis thaliana
  • sample-icon 165 Downloadable Samples
  • Technology Badge IconNextSeq 500

Description

A fundamental question in biology is how gene expression is regulated to give rise to a phenotype. However, transcriptional variability is rarely considered and could influence the relationship between genotype and phenotype. It is known in unicellular organisms that gene expression is often noisy rather than uniform and has been proposed to be beneficial when environmental conditions are unpredictable. However, little is known about transcriptional variability in multicellular organisms. Using transcriptomic approaches, we analysed gene expression variability over a 24 hours time-course between individual Arabidopsis thaliana plants growing in stable conditions. We identified hundreds of genes that exhibit high inter-individual variability and found that many are involved in environmental responses. We also identified factors that might facilitate gene expression variability, such as gene size, the number of transcription factors regulating a gene and the chromatin environment. These results will bring a new light into the impact of transcriptional variability in gene expression regulation in plants. Overall design: RNA-seq were generated for 14 individual seedlings for each of the 12 following time points: ZT2, ZT4, ZT6, ZT8, ZT10, ZT12 (just before dusk), ZT14, ZT16, ZT18, ZT20, ZT22 and ZT24 (just before dawn).

Publication Title

Widespread inter-individual gene expression variability in <i>Arabidopsis thaliana</i>.

Sample Metadata Fields

Specimen part, Subject, Time

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accession-icon GSE21611
Oscillating gene expression determines competence for periodic branching in the Arabidopsis root
  • organism-icon Arabidopsis thaliana
  • sample-icon 39 Downloadable Samples
  • Technology Badge Icon Affymetrix Arabidopsis ATH1 Genome Array (ath1121501)

Description

The Oscillation Zone (OZ) of unsynchronized roots was disected and divided into an upper (OZ2) and lower (OZ1) half .

Publication Title

Oscillating gene expression determines competence for periodic Arabidopsis root branching.

Sample Metadata Fields

Age, Specimen part

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accession-icon GSE103190
Genome-wide analysis between murine invariant NKT cells and CD4+ T cells
  • organism-icon Mus musculus
  • sample-icon 2 Downloadable Samples
  • Technology Badge IconIllumina MouseRef-8 v2.0 expression beadchip

Description

Analysis between two different types of T cells

Publication Title

Comparison of Invariant NKT Cells with Conventional T Cells by Using Gene Set Enrichment Analysis (GSEA).

Sample Metadata Fields

Sex, Specimen part

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accession-icon GSE59219
Intrinsic self-DNA triggers inflammatory disease dependent on STING
  • organism-icon Mus musculus
  • sample-icon 18 Downloadable Samples
  • Technology Badge IconIllumina MouseWG-6 v2.0 expression beadchip

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Intrinsic self-DNA triggers inflammatory disease dependent on STING.

Sample Metadata Fields

Specimen part

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accession-icon GSE59217
Intrinsic self-DNA triggers inflammatory disease dependent on STING (I)
  • organism-icon Mus musculus
  • sample-icon 12 Downloadable Samples
  • Technology Badge IconIllumina MouseWG-6 v2.0 expression beadchip

Description

Inflammatory diseases such as Aicardi-Goutieres Syndrome (AGS) and severe systemic lupus erythematosus (SLE) are generally lethal disorders that have been traced to defects in the exonuclease Trex1 (DNAseIII). Mice lacking Trex1 similarly die at an early age through comparable symptoms, including inflammatory myocarditis, through chronic activation of the STING (stimulator of interferon genes) pathway. Here we demonstrate that phagocytes rather than myocytes are predominantly responsible for causing inflammation, an outcome that could be alleviated following adoptive transfer of normal bone marrow into Trex1-/- mice. Trex1-/- macrophages did not exhibit significant augmented ability to produce pro-inflammatory cytokines compared to normal macrophages following exposure to STING-dependent activators, but rather appeared chronically stimulated by genomic DNA. These results shed molecular insight into inflammation and provide concepts for the design of new therapies.

Publication Title

Intrinsic self-DNA triggers inflammatory disease dependent on STING.

Sample Metadata Fields

Specimen part

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accession-icon GSE59218
Intrinsic self-DNA triggers inflammatory disease dependent on STING (II)
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge IconIllumina MouseWG-6 v2.0 expression beadchip

Description

Inflammatory diseases such as Aicardi-Goutieres Syndrome (AGS) and severe systemic lupus erythematosus (SLE) are generally lethal disorders that have been traced to defects in the exonuclease Trex1 (DNAseIII). Mice lacking Trex1 similarly die at an early age through comparable symptoms, including inflammatory myocarditis, through chronic activation of the STING (stimulator of interferon genes) pathway. Here we demonstrate that phagocytes rather than myocytes are predominantly responsible for causing inflammation, an outcome that could be alleviated following adoptive transfer of normal bone marrow into Trex1-/- mice. Trex1-/- macrophages did not exhibit significant augmented ability to produce pro-inflammatory cytokines compared to normal macrophages following exposure to STING-dependent activators, but rather appeared chronically stimulated by genomic DNA. These results shed molecular insight into inflammation and provide concepts for the design of new therapies.

Publication Title

Intrinsic self-DNA triggers inflammatory disease dependent on STING.

Sample Metadata Fields

Specimen part

View Samples
accession-icon GSE5430
Expression data from early Drosophila embryo
  • organism-icon Drosophila melanogaster
  • sample-icon 64 Downloadable Samples
  • Technology Badge Icon Affymetrix Drosophila Genome 2.0 Array (drosophila2)

Description

Translational control is critical for early Drosophila embryogenesis and is exerted mainly at the gene-specific level.

Publication Title

Global analyses of mRNA translational control during early Drosophila embryogenesis.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE107811
STING-Dependent Signaling Manifests IL-10 Controlled Inflammatory Colitis
  • organism-icon Mus musculus
  • sample-icon 21 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 2.0 ST Array (mogene20st)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

STING-Dependent Signaling Underlies IL-10 Controlled Inflammatory Colitis.

Sample Metadata Fields

Specimen part

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accession-icon GSE107810
Gene expression in the colon from IL10 KO mice
  • organism-icon Mus musculus
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 2.0 ST Array (mogene20st)

Description

That commensal bacteria can influence intestinal inflammation has been observed using other models of chronic colitis. Loss of IL-10, a major immunosuppressive cytokine, induces spontaneous colitis in mice. The incidence of spontaneous polyp formation in IL-10-deficient mice was also completely eliminated in the absence of STING

Publication Title

STING-Dependent Signaling Underlies IL-10 Controlled Inflammatory Colitis.

Sample Metadata Fields

Specimen part

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accession-icon GSE107809
Gene expression in murine embryonic fibroblasts stimulated with DNA or LPS
  • organism-icon Mus musculus
  • sample-icon 9 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 2.0 ST Array (mogene20st)

Description

MyD88 may play a direct role in STING-dependent signaling, or alternatively that STING-dependent pro-inflammatory cytokines may require downstream MyD88-dependent signaling to exert their effect.

Publication Title

STING-Dependent Signaling Underlies IL-10 Controlled Inflammatory Colitis.

Sample Metadata Fields

Specimen part

View Samples
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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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