refine.bio
  • Search
      • Normalized Compendia
      • RNA-seq Sample Compendia
  • Docs
  • About
  • My Dataset
github link
Showing
of 864 results
Sort by

Filters

Technology

Platform

accession-icon GSE43710
Type I and type III interferons drive redundant amplification loops to induce a transcriptional signature in influenza-infected airway epithelia
  • organism-icon Mus musculus
  • sample-icon 62 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Type I and type III interferons drive redundant amplification loops to induce a transcriptional signature in influenza-infected airway epithelia.

Sample Metadata Fields

Specimen part

View Samples
accession-icon GSE43708
Expression data from Influenza A infected mouse primary tracheal epithelial cell cultures (MTEC), from wild-type, IFNAR1-/-, IL28Ra-/- and IFNAR1-/- IL28Ra-/- double ko
  • organism-icon Mus musculus
  • sample-icon 40 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

We used microarrays to detail the global programme of gene expression in response to Influenza A (PR8) infection

Publication Title

Type I and type III interferons drive redundant amplification loops to induce a transcriptional signature in influenza-infected airway epithelia.

Sample Metadata Fields

Specimen part

View Samples
accession-icon GSE43709
Expression data from Influenza A infected mouse primary tracheal epithelial cell cultures (MTEC), from both wild-type and MAVS-/- mice
  • organism-icon Mus musculus
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

We used microarrays to detail the global programme of gene expression in response to Influenza A (PR8) infection

Publication Title

Type I and type III interferons drive redundant amplification loops to induce a transcriptional signature in influenza-infected airway epithelia.

Sample Metadata Fields

Specimen part

View Samples
accession-icon GSE43707
Expression data from Influenza A infected mouse primary tracheal epithelial cell cultures (MTEC)
  • organism-icon Mus musculus
  • sample-icon 10 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

We used microarrays to detail the global programme of gene expression in response to Influenza A (PR8) infection

Publication Title

Type I and type III interferons drive redundant amplification loops to induce a transcriptional signature in influenza-infected airway epithelia.

Sample Metadata Fields

Specimen part

View Samples
accession-icon GSE48970
Contribution of the STAT1alpha and STAT1beta isoforms to IFN-gamma mediated innate immunity
  • organism-icon Mus musculus
  • sample-icon 48 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

The transcription factor STAT1 is essential for interferon- (IFN) mediated protective immunity in humans and mice. Two splice isoforms of STAT1, STAT1 and STAT1, differ with regard to a C-terminal transactivation domain, which is absent in STAT1. Dimers of STAT1 are therefore considered transcriptionally inactive and potential competitive inhibitors of STAT1. Contrasting this view, generation and analysis of mice deficient for either STAT1 or STAT1 demonstrated transcriptional activity of the STAT1 isoform and its enhancement of innate immunity. Gene expression profiling in primary cells revealed overlapping, but also non-redundant and gene-specific activities of STAT1 and STAT1 in response to IFN. Consistently, both isoforms mediated protective, IFN-dependent immunity against the bacterium Listeria monocytogenes, although with remarkably different efficiency. In contrast, STAT1 and STAT1 were largely redundant for transcriptional responses to IFN/ and for IFN/-dependent antiviral activity. Collectively, our data shed new light on how STAT1 isoforms contribute to antimicrobial immunity.

Publication Title

STAT1β is not dominant negative and is capable of contributing to gamma interferon-dependent innate immunity.

Sample Metadata Fields

Specimen part

View Samples
accession-icon GSE67858
Host microbiota constantly control maturation and function of microglia in the central nervous system
  • organism-icon Mus musculus
  • sample-icon 32 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 2.1 ST Array (mogene21st)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Host microbiota constantly control maturation and function of microglia in the CNS.

Sample Metadata Fields

Specimen part, Treatment

View Samples
accession-icon GSE67857
Host microbiota constantly control maturation and function of microglia in the central nervous system (part 2)
  • organism-icon Mus musculus
  • sample-icon 20 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 2.1 ST Array (mogene21st)

Description

As tissue macrophages of the central nervous system (CNS), microglia are critically involved in diseases of the CNS. However, it remains unknown what controls their maturation and activation under homeostatic conditions. Here we reveal significant contributions of the host microbiota to microglia homeostasis as germ-free (GF) mice displayed global defects in microglia with altered cell proportions and an immature phenotype leading to impaired innate immune responses. Temporal eradication of host microbiota severely changed microglia properties. Limited microbiota complexity also resulted in defective microglia. In contrast, recolonization with a complex microbiota partially restored microglia features. We determined that short-chain fatty acids (SCFA), microbiota-derived bacterial fermentation products, regulate microglia homeostasis. Accordingly, mice deficient for the SCFA receptor FFAR2 mirrored microglia defects found under GF conditions. These findings reveal that host bacteria vitally regulate microglia maturation and function, whereas microglia impairment can be restored to some extent by complex microbiota.

Publication Title

Host microbiota constantly control maturation and function of microglia in the CNS.

Sample Metadata Fields

Specimen part, Treatment

View Samples
accession-icon GSE62201
Host microbiota constantly control maturation and function of microglia in the central nervous system (part 1)
  • organism-icon Mus musculus
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 2.1 ST Array (mogene21st)

Description

As tissue macrophages of the central nervous system (CNS), microglia are critically involved in diseases of the CNS. However, it remains unknown what controls their maturation and activation under homeostatic conditions. Here we reveal significant contributions of the host microbiota to microglia homeostasis as germ-free (GF) mice displayed global defects in microglia with altered cell proportions and an immature phenotype leading to impaired innate immune responses. Temporal eradication of host microbiota severely changed microglia properties. Limited microbiota complexity also resulted in defective microglia. In contrast, recolonization with a complex microbiota partially restored microglia features. We determined that short-chain fatty acids (SCFA), microbiota-derived bacterial fermentation products, regulate microglia homeostasis. Accordingly, mice deficient for the SCFA receptor FFAR2 mirrored microglia defects found under GF conditions. These findings reveal that host bacteria vitally regulate microglia maturation and function, whereas microglia impairment can be restored to some extent by complex microbiota.

Publication Title

Host microbiota constantly control maturation and function of microglia in the CNS.

Sample Metadata Fields

Specimen part, Treatment

View Samples
accession-icon GSE1907
Sarcoidosis + Follow-up study
  • organism-icon Homo sapiens
  • sample-icon 32 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U95A Array (hgu95a)

Description

Sarcoidosis + Follow-up 6 month after

Publication Title

Functional genomics and prognosis in sarcoidosis--the critical role of antigen presentation.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon GSE29832
Expression data from pure/mixed blood and breast to test feasability of deconvolution of clinical samples
  • organism-icon Homo sapiens
  • sample-icon 14 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Samples collected from human subjects in clinical trials possess a level of complexity, arising from multiple cell types, that can obfuscate the analysis of data derived from them. Blood, for example, contains many different cell types that are derived from a distinct lineage and carry out a different immunological purpose. Failure to identify, quantify, and incorporate sources of heterogeneity into an analysis can have widespread and detrimental effects on subsequent statistical studies.

Publication Title

Optimal deconvolution of transcriptional profiling data using quadratic programming with application to complex clinical blood samples.

Sample Metadata Fields

Sex, Specimen part

View Samples
...

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)

fund-icon Fund the CCDL

Developed by the Childhood Cancer Data Lab

Powered by Alex's Lemonade Stand Foundation

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.

BSD 3-Clause LicensePrivacyTerms of UseContact