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accession-icon GSE18323
Expression data from a malaria vaccine trial (HG-U133A2.0 and U133 Plus 2.0)
  • organism-icon Homo sapiens
  • sample-icon 254 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Volunteers were assessed at study entry, the day of the third vaccination and 24, 72 hours, two weeks after vaccination, and 5 days after challenge. 13/39 vaccinees were protected and 26/39 were not protected. Eleven vaccinees exhibited delayed onset of parasitemia. All infectivity controls developed parasitemia. Prediction Analysis of Microarrays (PAM-R) identified genes corresponding with protection. Gene Set Enrichment Analysis (GSEA) identified sets of genes associated with protection after the third immunization, before challenge.

Publication Title

Expression of genes associated with immunoproteasome processing of major histocompatibility complex peptides is indicative of protection with adjuvanted RTS,S malaria vaccine.

Sample Metadata Fields

Specimen part

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accession-icon GSE5418
Gene Expression Analysis in Malaria Infection
  • organism-icon Homo sapiens
  • sample-icon 71 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A Array (hgu133a)

Description

Using genome-wide expression profiles from persons either experimentally challenged with malaria-infected mosquitoes or naturally-infected with Plasmodium falciparum malaria, we present details of the transcriptional changes that occur with infection and that are either commonly shared between subjects with pre-symptomatic and clinically apparent malaria or that distinguish these two groups. Our findings confirm and extend aspects of the earliest responses to malaria infection at the molecular level and which may be informative in elucidating how innate and adaptive immune responses may be modulated in different stages of infection.

Publication Title

No associated publication

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE33325
Gene expression changes in human cardiomyocytes exposed to VX (O-ethyl S-[2-(diisopropylamino)ethyl] methylphosphonothiolate)
  • organism-icon Homo sapiens
  • sample-icon 38 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Organophosphorus compounds induce cardiotoxicity through currently unknown mechanisms, which need to be unraveled by a comprehensive and systematic approach such as genome-wide gene expression analysis.

Publication Title

No associated publication

Sample Metadata Fields

Specimen part

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accession-icon GSE33109
Gene expression changes in human neural cells exposed to VX (O-ethyl S-[2-(diisopropylamino)ethyl] methylphosphonothiolate)
  • organism-icon Homo sapiens
  • sample-icon 36 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Organophosphorus compounds may induce neurotoxicity through mechanisms other than the cholinergic pathway, which need to be unraveled by a comprehensive and systematic approach such as genome-wide gene expression analysis.

Publication Title

Toxicogenomic studies of human neural cells following exposure to organophosphorus chemical warfare nerve agent VX.

Sample Metadata Fields

Specimen part

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accession-icon GSE7157
Infection of Macaques with SIVmac251 in vivo
  • organism-icon Macaca fascicularis
  • sample-icon 26 Downloadable Samples
  • Technology Badge Icon Affymetrix Rhesus Macaque Genome Array (rhesus)

Description

Viral infection results in an overall downregulation of gene expression that is greatest by the viral set point. Of the 3647 genes downregulated at the viral set point, 1033 are upregulated as the result of successful ARV treatment

Publication Title

No associated publication

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE57605
Inflammation-Driven Carcinogenesis is Mediated through STING
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge IconIllumina MouseWG-6 v2.0 expression beadchip

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Inflammation-driven carcinogenesis is mediated through STING.

Sample Metadata Fields

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 GSE33606
Gene expression changes in human hepatocytes exposed to VX (O-ethyl S-[2-(diisopropylamino)ethyl] methylphosphonothiolate)
  • organism-icon Homo sapiens
  • sample-icon 14 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Organophosphorus compounds induce hepatotoxicity through currently unknown mechanisms, which need to be unraveled by a comprehensive and systematic approach such as genome-wide gene expression analysis.

Publication Title

No associated publication

Sample Metadata Fields

Specimen part, Time

View Samples
accession-icon GSE57603
Inflammation-Driven Carcinogenesis is Mediated through STING [MEFs]
  • organism-icon Mus musculus
  • sample-icon 5 Downloadable Samples
  • Technology Badge IconIllumina MouseWG-6 v2.0 expression beadchip

Description

Chronic stimulation of innate immune pathways by microbial agents or damaged tissue is known to promote inflammation-driven tumorigenesis by unclarified mechanisms1-3. Here we demonstrate that mutagenic 7,12-dimethylbenz(a)anthracene (DMBA), etoposide or cisplatin induces nuclear DNA leakage into the cytosol to intrinsically activate STING (Stimulator of Interferon Genes) dependent cytokine production. Inflammatory cytokine levels were subsequently augmented in a STING-dependent extrinsic manner by infiltrating phagocytes purging dying cells. Consequently, STING-/- mice, or wild type mice adoptively transferred with STING-/- bone marrow, were almost completely resistant to DMBA-induced skin carcinogenesis compared to their wild type counterparts. Our data emphasizes, for the first time, a role for STING in the induction of cancer, sheds significant insight into the causes of inflammation-driven carcinogenesis, and may provide therapeutic strategies to help prevent malignant disease

Publication Title

Inflammation-driven carcinogenesis is mediated through 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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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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