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accession-icon GSE48210
Kinetic analysis of the response to anti-CD3 in conventional and regulatory CD4+ T cells, in mice and in vitro.
  • organism-icon Mus musculus
  • sample-icon 42 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

Several clinical trials have shown anti-CD3 treatment to be a promising therapy for autoimmune diabetes, but its mechanism of action remains unclear. Foxp3+ regulatory T (Treg) cells are likely to be involved, and we have shown a strong effect of anti-CD3 on homeostatic control of CD4+ FoxP3+ regulatory T (Treg) cells. To analyze the early consequences of anti-CD3 treatment, we sorted and profiled Treg and conventional CD4+ T (Tconv) cells in the first hours and days after anti-CD3 treatment of NOD mice. In practice, NOD mice carrying the Foxp3-GFP reporter were treated with anti-CD3 mAb KT3 (50 ug iv) and CD4+ T cells were sorted from pooled spleen and lymph nodes after 2, 8, 24 and 72 hrs, separating Treg and Tconv cells on the basis of GFP expression. Anti-CD3 treatment led to a transient transcriptional response, terminating faster than most antigen-induced responses. Most transcripts were similarly induced in Treg and Tconv cells, but several were differential, in particular those encoding the IL7 receptor (IL7R) and transcription factors Id2/3 and Gfi1, upregulated in Treg but repressed in Tconv cells. In parallel experiments, we tested the effect of soluble anti-CD3 added to cultures of fresh splenocytes, sorting Treg and Tconv cells at the same time points. Many of the anti-CD3 elicited changes, and of the differential response observed in vivo, were also observed in vitro. Two independent replicate series; Treg and Tconv samples abbreviated TR and TC, respectively. Keywords: Transcriptional activation, TCR

Publication Title

Differential response of regulatory and conventional CD4⁺ lymphocytes to CD3 engagement: clues to a possible mechanism of anti-CD3 action?

Sample Metadata Fields

Sex, Age

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accession-icon GSE54534
Expression data provoked by H2O2 from plastid or peroxisomal origin
  • organism-icon Arabidopsis thaliana
  • sample-icon 25 Downloadable Samples
  • Technology Badge Icon Affymetrix Arabidopsis ATH1 Genome Array (ath1121501)

Description

Reactive oxygen species (ROS) are key signalling molecules that regulate growth and development and coordinate responses to biotic and abiotic stresses. ROS homeostasis is controlled through a complex network of ROS production and scavenging enzymes. Recently, the first genes involved in ROS perception and signal transduction have been identified and, currently, we are facing the challenge to uncover the other players within the ROS regulatory gene network. The specificity of ensuing cellular responses depends on the type of ROS and their subcellular production sites. Various experimental systems, including catalase-deficient plants, in combination with genome-wide expression studies demonstrated that increased hydrogen peroxide (H2O2) levels significantly affect the transcriptome of plants and are capable of launching both defence responses and cell death events.

Publication Title

Spatial H2O2 signaling specificity: H2O2 from chloroplasts and peroxisomes modulates the plant transcriptome differentially.

Sample Metadata Fields

Age, Specimen part

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accession-icon SRP107747
Specific labeling of stem cell activity in human colorectal organoids using an ASCL2-responsive minigene
  • organism-icon Homo sapiens
  • sample-icon 18 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

Organoid technology provides the possibility to culture human colon tissue and patient-derived colorectal cancers (CRC) while maintaining all functional and phenotypic characteristics. Labeling of human colon stem cells (CoSCs), especially in normal and benign tumor organoids, is challenging and therefore limits usability of multi-patient organoid libraries for CoSC research. Here, we developed STAR (STem cell Ascl2 Reporter), a minimal enhancer/promoter element that reports transcriptional activity of ASCL2, a master regulator of LGR5+ CoSC fate. Among others via lentiviral infection, STAR minigene labels stem cells in normal as well as in multiple engineered and patient-derived CRC organoids of different stage and genetic make-up. STAR revealed that stem cell driven differentiation hierarchies and the capacity of cell fate plasticity (de-differentiation) are present at all stages of human CRC development. The flexible and user-friendly nature of STAR applications in combination with organoid technology will facilitate basic research on human adult stem cell biology. Overall design: Cells from different colon organoid types were FACS sorted for stem STemness Ascl2 Reporter activity for transcriptome profiling by RNA-seq.

Publication Title

Specific Labeling of Stem Cell Activity in Human Colorectal Organoids Using an ASCL2-Responsive Minigene.

Sample Metadata Fields

Subject

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accession-icon SRP028138
Transcriptional profile in the colon in response to C. rodentium infection.
  • organism-icon Mus musculus
  • sample-icon 20 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

The identification of Atg16L1 as a susceptibility gene has implicated antibacterial autophagy in the pathogenesis of Crohn''s disease, a major type of inflammatory bowel disease (IBD). However, the role of Atg16L1 during extracellular bacterial infections of the intestine has not been sufficiently examined and compared to the function of other IBD susceptibility genes such as Nod2. We now find that Atg16L1 mutant mice are extraordinarily resistant to intestinal disease induced by the model bacterial pathogen Citrobacter rodentium. We further demonstrate that Atg16L1 deficiency alters the intestinal environment to mediate an enhanced immune response that is dependent on monocytic cells, and that Atg16L1/Nod2 double mutant mice lose this advantage. These results reveal an unappreciated immuno-suppressive function of an IBD gene, and raise the possibility that gene variants that affect the autophagy pathway were evolutionarily maintained to protect against certain life-threatening infections. Overall design: Twenty samples have been analyzed. All are colonic tissue from mice. Controls are uninfected WT mice, uninfected Atg16L1 mutant mice (Atg16L1HM) (n=3/genotype). Treatment conditions are tissue from WT and Atg16L1 mutant mice 6 days after C. rodentium infection (n=4/genotype) and 15 days after infection (n=3/genotype).

Publication Title

A deficiency in the autophagy gene Atg16L1 enhances resistance to enteric bacterial infection.

Sample Metadata Fields

Specimen part, Subject

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accession-icon GSE27159
Expression profiling of the murine neural crest precursor cell line, JoMa1
  • organism-icon Mus musculus
  • sample-icon 8 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

JoMa1 cells are pluripotent precursor cells, derived from the neural crest of mice transgenic for tamoxifen-inducible c-Myc. Following transfection with a cDNA encoding for MYCN, cells become immortlized even in the absence of tamoxifen.

Publication Title

MYCN and ALKF1174L are sufficient to drive neuroblastoma development from neural crest progenitor cells.

Sample Metadata Fields

Specimen part, Cell line

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accession-icon GSE61560
Gene expression analysis of CD11c+ splenic DCs day 7 after allo-HSCT.
  • organism-icon Mus musculus
  • sample-icon 7 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430A 2.0 Array (mouse430a2)

Description

The goal of our study is to determine whether Atg16L1 deficiency leads to differences in the transcriptional profile of CD11c+ Dendritic Cells, ultimately leading to an increased inflammatory phenotype.

Publication Title

Autophagy gene Atg16L1 prevents lethal T cell alloreactivity mediated by dendritic cells.

Sample Metadata Fields

Specimen part

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accession-icon GSE61559
Gene expression analysis of CD11c+ splenic DCs.
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430A 2.0 Array (mouse430a2)

Description

The goal of our study is to determine whether Atg16L1 deficiency leads to differences in the transcriptional profile of CD11c+ Dendritic Cells, ultimately leading to an increased inflammatory phenotype.

Publication Title

Autophagy gene Atg16L1 prevents lethal T cell alloreactivity mediated by dendritic cells.

Sample Metadata Fields

Age, Specimen part

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accession-icon GSE61561
CD11c+ splenic DCs
  • organism-icon Mus musculus
  • sample-icon 3 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430A 2.0 Array (mouse430a2)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Autophagy gene Atg16L1 prevents lethal T cell alloreactivity mediated by dendritic cells.

Sample Metadata Fields

Age, Specimen part

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accession-icon GSE139334
Gene expression analysis of fibroblasts of systemic sclerosis patients silenced for lncRNA H19X
  • organism-icon Homo sapiens
  • sample-icon 12 Downloadable Samples
  • Technology Badge IconIllumina HumanHT-12 V4.0 expression beadchip

Description

LncRNA H19X was silienced in dermal fibroblats of systemic sclerosis patients with antisense oligonuclotides. The hypothesis tested in the present study was that H19X is an important factor in the development of TGFb-driven fibrosis. Results provide important information about the role H19X in fibroblasts in particolar on extracellular matrix production and cell cycle regulation.

Publication Title

Long noncoding RNA H19X is a key mediator of TGF-β-driven fibrosis.

Sample Metadata Fields

Specimen part, Disease, Disease stage, Treatment

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accession-icon GSE15602
Differential gene expression in RA synovial biopsies from responders versus non-responders to adalimumab therapy
  • organism-icon Homo sapiens
  • sample-icon 9 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

TNF antagonists are routinely used in severe rheumatoid arthritis (RA) patients who failed conventional DMARD therapy. According to large clinical trials, the three available drugs (adalimumab, infliximab and etanercept) display similar effects in terms of efficacy, tolerability and side effects. These studies also indicate that about 25% of RA patients treated with TNF-antagonists do not display any significant clinical improvement.

Publication Title

Gene expression profiling in the synovium identifies a predictive signature of absence of response to adalimumab therapy in rheumatoid arthritis.

Sample Metadata Fields

Specimen part, Disease

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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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