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accession-icon GSE1867
mouse corneal stromal cells
  • organism-icon Mus musculus
  • sample-icon 14 Downloadable Samples
  • Technology Badge Icon Affymetrix Murine Genome U74A Version 2 Array (mgu74av2)

Description

To elucidate biological processes underlying the keratocyte, fibroblast, and myofibroblast phenotypes of corneal stromal cells, the gene expression patterns of these primary cultures from mouse cornea were compared with those of the adult and 10-day postnatal mouse cornea.

Publication Title

Microarray studies reveal macrophage-like function of stromal keratocytes in the cornea.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE53349
CD8+ T cells during acute viral respiratory infection are uniquely differentiated and regulated by multiple inhibitory receptors
  • organism-icon Mus musculus
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.1 ST Array (mogene11st)

Description

Acute viral infection typically generates functional effector CD8+ T cells that aid in pathogen clearance. However, during acute viral lower respiratory infection (LRI), lung CD8+ T cells are functionally impaired and do not optimally control viral replication, while spleen CD8+ T cells specific for the same viral epitopes remain fully functional. To better understand the mechanisms governing lung CD8+ T cell impairment, we used flow cytometry to sort anti-viral CD8+ T cells during viral LRI. Lung and spleen cells were stained with MHC-class I tetramers representing the immunodominant anti-viral CD8+ T cell epitope. We then sorted to high purity: nave CD8+ T cells, spleen epitope-specific CD8+ T cells, lung epitope-specific CD8+ cells and secondary infection lung epitope-specific CD8+ T cells. We then performed a genome wide transcriptional analysis of these cells to characterize the gene expression profile of lung CD8+ T cell impairment.

Publication Title

Acute Viral Respiratory Infection Rapidly Induces a CD8+ T Cell Exhaustion-like Phenotype.

Sample Metadata Fields

Sex, Specimen part

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accession-icon SRP007825
Small RNA sequencing in normal and psoriatic skin
  • organism-icon Homo sapiens
  • sample-icon 66 Downloadable Samples
  • Technology Badge IconIllumina Genome Analyzer IIx

Description

We report the application of Illumina small RNA sequencing to normal human skin, as well as uninvolved and involved psoriatic skin. By obtaining over 600 million qualified reads from 20 healthy controls and 47 psoriasis biopsies (uninvolved/involved), we have generated a complete small RNA profile in normal and diseased human skin, with particular emphasis on miRNAs. We report the discovery of 284 putative novel miRNAs as well as 98 differentially expressed miRNAs in psoriatic skin. Overall design: miRNA discovery and expression profiling in 67 normal and psoriatic human skin biopsies

Publication Title

Deep sequencing of small RNAs from human skin reveals major alterations in the psoriasis miRNAome.

Sample Metadata Fields

Specimen part, Disease, Disease stage, Subject

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accession-icon GSE73535
Histone Deacetylase 3
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Histone Deacetylase 3 Is Required for Efficient T Cell Development.

Sample Metadata Fields

Specimen part

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accession-icon GSE15500
Analysis of differences in gene expression due to small adaptive mutations in RNA polymerase B' subunit (rpoC)
  • organism-icon Escherichia coli
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix E. coli Genome 2.0 Array (ecoli2)

Description

Studies of the RNA polymerase-binding molecule ppGpp in bacteria and plants have shown that changes to the kinetics of the RNA polymerase can have dramatic biological effects in the short-term as a stress response. Here we describe the reprogramming of the kinetic parameters of the RNAP through mutations arising during laboratory adaptive evolution of Escherichia coli in minimal media. The mutations cause a 10- to 30-fold decrease in open complex stability at a ribosomal promoter and approximately a 10-fold decrease in transcriptional pausing in the his operon. The kinetic changes coincide with large scale transcriptional changes, including strong downregulation of motility, acid-resistance, fimbria, and curlin genes which are observed in site-directed mutants containing the RNA polymerase mutations as well as the evolved strains harboring the mutations. Site-directed mutants also grow 60% faster than the parent strain and convert the carbon-source 15% to 35% more efficiently to biomass. The results show that long-term adjustment of the kinetic parameters of RNA polymerase through mutation can be important for adaptation to a condition.

Publication Title

RNA polymerase mutants found through adaptive evolution reprogram Escherichia coli for optimal growth in minimal media.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon SRP070081
RNA-Seq of SLNCR1 over-expression in the melanoma cell line A375
  • organism-icon Homo sapiens
  • sample-icon 8 Downloadable Samples
  • Technology Badge IconNextSeq500

Description

RNA-Seq was used to profile transcriptional changes induced by overexpression of the long non-coding RNA SLNCR1, as well as mutant version SLNCR1 delta conserved and SLNCR1 conserved. Overall design: The A375 melanoma cell line was transfected with pcDNA3.1 (-) expressing either full length SLNCR1, SLNCR1 delta conserved, or SLNCR1 conserved.

Publication Title

The lncRNA SLNCR1 Mediates Melanoma Invasion through a Conserved SRA1-like Region.

Sample Metadata Fields

No sample metadata fields

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accession-icon SRP063574
Histone Deacetylase 3 is required for efficient T cell development
  • organism-icon Mus musculus
  • sample-icon 8 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

Hdac3 is an important target of HDAC inhibitors used in the treatment of cutaneous T cell lymphoma. In order to gain an understanding of Hdac3 function in T cells,we deleted Hdac3 from early mouse thymocytes using LCK-Cre. Hdac3 deletion resulted in a loss of single positive thymocytes due to a defect in positive selection at the double positive (DP) stage of thymocyte development. To better characterize this defect, we sorted the DP1 and DP2 populations to for gene expression profiling. Overall design: Total RNA was extracted from DP1 (GFP+CD4+CD8+CD5loTCRblo) or DP2 (GFP+CD4+CD8+CD5hiTCRbint) thymocytes isolated by FACS from Hdac3+/+ or Hdac3F/F LCK-Cre+ animals. Libraries were constructed from rRNA-depleted total RNA pools to identify altered gene expression in DP populations following Hdac3 deletion.

Publication Title

Histone Deacetylase 3 Is Required for Efficient T Cell Development.

Sample Metadata Fields

Specimen part, Cell line, Subject

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accession-icon SRP070082
RNA-Seq of siRNA-mediated knockdown of the lncRNA SLNCR1 in WM1976 melanoma cells
  • organism-icon Homo sapiens
  • sample-icon 4 Downloadable Samples
  • Technology Badge IconNextSeq500

Description

RNA-Seq was used to profile transcriptional changes induced by siRNA knockdown of the long non-coding RNA SLNCR1. Overall design: The WM1976 melanoma short-term culture was transfected with either scrambled or SLNCR1-targeting siRNAs

Publication Title

The lncRNA SLNCR1 Mediates Melanoma Invasion through a Conserved SRA1-like Region.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon GSE6789
response to IL-1b of WT and IRAK4 kinase dead mouse embryonic fibroblasts
  • organism-icon Mus musculus
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

IRAK-4 is an essential component of the signal transduction complex downstream of the IL-1- and Toll-like receptors. Though regarded as the first kinase in the signaling cascade, the role of IRAK-4 kinase activity versus its scaffold function is still controversial. In order to investigate the role of IRAK-4 kinase function in vivo, knock-in mice were generated by replacing the wild type IRAK-4 gene with a mutant gene encoding kinase deficient IRAK-4 protein (IRAK-4 KD). Analysis of embryonic fibroblasts and macrophages obtained from IRAK-4 KD mice with a number of experimental techniques demonstrated that they greatly lack responsiveness to stimulation with IL-1b or a Toll-like receptor 7 (TLR7) agonist. One of the techniques used, microarray analysis, identified IRAK-4 kinase-dependent IL-1b response genes in mouse embryonic fibroblasts and revealed that the induction of IL-1b-responsive mRNAs was largely ablated in IRAK-4 KD cells. In summary, our results suggest that IRAK-4 kinase activity plays a critical role in IL-1R/TLR7-mediated induction of inflammatory responses.

Publication Title

IRAK-4 kinase activity is required for interleukin-1 (IL-1) receptor- and toll-like receptor 7-mediated signaling and gene expression.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE39469
Expression data from proliferating and senescent murine hepatic stellate cells
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

The p53 protein is a cell-autonomous tumor suppressor that restricts malignant transformation by triggering cell cycle exit or apoptosis. p53 also promotes cellular senescence, a program that triggers a stable cell cycle arrest and can modify the tissue microenvironment through its effect on cell membrane and secretory proteins. Here we show that specific ablation of p53 in hepatic stellate cells, which undergo a process of proliferation and senescence in the fibrogenic response to liver damage, enhances liver cirrhosis, reduces survival and increases the malignant transformation of adjacent epithelial cells into hepatocellular carcinoma. This p53-dependent senescence program involves the release of secreted proteins which skew macrophages into a tumor-inhibiting M1-state that can eliminate senescent stellate cells. In contrast, p53-deficient stellate cells secrete factors that promote M2 polarization, which is pro-tumorigenic. Our study reveals that p53 can exert a non-cell-autonomous tumor suppressor response and suggests that this occurs, in part, by its ability to influence macrophage polarization.

Publication Title

Non-cell-autonomous tumor suppression by p53.

Sample Metadata Fields

Specimen part, Treatment

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

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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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