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accession-icon SRP090558
Interferon regulated genes in mouse intestine after irradiation and prophylactic Rig-I activation
  • organism-icon Mus musculus
  • sample-icon 45 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

As RIG-I activation induces potent IFN-I responses,we analyzed the role of IFN-I in intestinal tissue protection and prevention of GVHD. We performed RNA sequencing with tissue samples from SI of WT mice that received TBI -/+ previous 3pRNA treatment and -/+ antibody-mediated blockade of IFNAR. Application of 3pRNA before TBI resulted in a significant increase of IFN-inducible genes in the SI as compared to solely irradiated mice. Blockade of IFNAR signaling abrogated 3pRNA-mediated up-regulation of IFN-induced genes, demonstrating that RIG-I-induced gene-regulation depends on IFN-I. Overall design: Balb/c mice were solely irradiated (9Gy) (n=3), pretreated with Rig-I agonist 3pRNA prior (d-1) to irradiation (n=3) or pre-treated with 3pRNA (d-1) + anti-IFNaR1 blocking antibody (d-2) prior to irradiation (n=3). RNA from small intestines was isolated 12h after irradiation and used for RNA sequencing.

Publication Title

RIG-I/MAVS and STING signaling promote gut integrity during irradiation- and immune-mediated tissue injury.

Sample Metadata Fields

Cell line, Subject

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accession-icon GSE106982
Production of BMP4 by endothelial cells is crucial for endogenous thymic regeneration
  • organism-icon Mus musculus
  • sample-icon 13 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

Production of BMP4 by endothelial cells is crucial for endogenous thymic regeneration.

Sample Metadata Fields

Sex, Specimen part

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accession-icon GSE106981
Expression data from thymic non-hematopoietic stromal cells after damage
  • organism-icon Mus musculus
  • sample-icon 9 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

The thymus is extremely sensitive to damage but also has a remarkable ability to repair itself. However, the mechanisms underlying this endogenous regeneration remain poorly understood and this capacity diminishes considerably with age. To identify alternate regeneration pathways in the thymus, we performed an unbiased transcriptome analysis of the non-hematopoietic (CD45-) stromal cell compartment of the thymus, which is less sensitive to thymic damage compared to the CD45+ hematopoietic compartment.

Publication Title

Production of BMP4 by endothelial cells is crucial for endogenous thymic regeneration.

Sample Metadata Fields

Sex, Specimen part

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accession-icon GSE106980
Expression data from thymic endothelial cells after damage
  • organism-icon Mus musculus
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

The thymus is extremely sensitive to damage but also has a remarkable ability to repair itself. However, the mechanisms underlying this endogenous regeneration remain poorly understood and this capacity diminishes considerably with age. To identify alternate regeneration pathways in the thymus, we performed an unbiased transcriptome analysis of the non-hematopoietic (CD45-) stromal cell compartment of the thymus, which is less sensitive to thymic damage compared to the CD45+ hematopoietic compartment.

Publication Title

Production of BMP4 by endothelial cells is crucial for endogenous thymic regeneration.

Sample Metadata Fields

Sex, Specimen part

View Samples
accession-icon GSE8187
Adaptation of S. cerevisiae to fermentative conditions
  • organism-icon Saccharomyces cerevisiae
  • sample-icon 8 Downloadable Samples
  • Technology Badge Icon Affymetrix Yeast Genome S98 Array (ygs98)

Description

The capacity of respiring cultures of Saccharomyces cerevisiae to instantaneously switch to fast alcoholic fermentation upon a transfer to anaerobic sugar-excess conditions is a key characteristic of Saccharomyces cerevisiae in many of its industrial applications. This transition was studied by exposing aerobic glucose-limited chemostat cultures grown at a low specific growth rate to two simultaneous perturbations: oxygen depletion and relief of glucose limitation. This shift towards fully fermentative conditions caused a massive transcriptional response, where one third of all genes within the genome were transcribed differentially. During the first 30 min, most of these changes were driven by relief from glucose limitation. An anaerobic induction response was only observed after the initial response to glucose excess. By comparing this study with public datasets representing dynamic and steady conditions, 14 up-regulated and 11 down-regulated genes were determined to be anaerobiosis specific and can therefore be use as signature transcripts for anaerobicity under dynamic as well as under steady state conditions

Publication Title

New insights into the Saccharomyces cerevisiae fermentation switch: dynamic transcriptional response to anaerobicity and glucose-excess.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE9644
Glucose Pulse to sfp1delta continuous cultures
  • organism-icon Saccharomyces cerevisiae
  • sample-icon 26 Downloadable Samples
  • Technology Badge Icon Affymetrix Yeast Genome S98 Array (ygs98)

Description

The Saccharomyces cerevisiae SFP1 is required for proper regulation of ribosome biogenesis and cell size in response to nutrients. A mutant deleted for SFP1 shows specific traits among which a slow growth phenotype, which is particularly evident during growth on glucose. To assess the effects of nutrients on the activity of Sfp1 independent by growth rate related feedback we grew an sfp1 mutant and its isogenic reference strain in chemostat cultures, at the same specific growth rate, under glucose/ethanol-limitation. Our data show that Sfp1 is involved in the modulation of cell size and RiBi gene expression and that these two functions are differently influenced by nutrients.

Publication Title

Saccharomyces cerevisiae SFP1: at the crossroads of central metabolism and ribosome biogenesis.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE90607
Fibrostenotic phenotype of fibroblasts in Crohn's disease is dependent on tissue stiffness and reversed by LOX inhibition
  • organism-icon Homo sapiens
  • sample-icon 24 Downloadable Samples
  • Technology Badge IconIllumina HumanHT-12 V4.0 expression beadchip

Description

The results of this study indicate that stenotic fibroblasts exhibit an aberrant response to tissue stiffness with reduced MMP activity, leading to a perpetuous vicious circle of ever more fibrosis formation. Altering the microenvironment by LOX inhibition increases MMP activity and decreases ECM contraction, resulting in a potential anti-fibrotic agent for Crohns disease.

Publication Title

Fibrostenotic Phenotype of Myofibroblasts in Crohn's Disease is Dependent on Tissue Stiffness and Reversed by LOX Inhibition.

Sample Metadata Fields

Sex, Specimen part, Disease, Subject

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accession-icon GSE28466
Induction of ER stress in the colon cancer cell line LS174 with SubAB
  • organism-icon Homo sapiens
  • sample-icon 6 Downloadable Samples
  • Technology Badge IconIllumina HumanHT-12 V3.0 expression beadchip

Description

To assess the effect of activation of the unfolded protein response (UPR) in colon cancer cell lines, we treated cells with the AB5 subtilase cytotoxin (SubAB). This proteolytically cleaves the 78-kDa glucose-regulated protein (GRP78; also known as HSPA5 or BiP) inside the endoplasmic reticulum. We find that the WNT signaling pathway is highly affected upon treatment with SubAB.

Publication Title

ER stress causes rapid loss of intestinal epithelial stemness through activation of the unfolded protein response.

Sample Metadata Fields

Specimen part, Cell line, Treatment

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accession-icon GSE103172
Indian Hedgehog suppresses a stromal cell driven intestinal immune response
  • organism-icon Mus musculus
  • sample-icon 9 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

Indian Hedgehog Suppresses a Stromal Cell-Driven Intestinal Immune Response.

Sample Metadata Fields

Specimen part, Time

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accession-icon GSE135015
Chimeric Antigen Receptor-Induced Bcl11b Suppression Propagates Natural Killer-Like Cell Development
  • organism-icon Homo sapiens
  • sample-icon 11 Downloadable Samples
  • Technology Badge Icon Affymetrix Clariom S Human array (clariomshuman)

Description

The transcription factor B Cell CLL/Lymphoma 11B (BCL11B) is indispensable for T lineage development of lymphoid progenitors. Here we show that chimeric antigen receptor (CAR) expression early in ex vivo generated lymphoid progenitors suppresses Bcl11b, leading to suppression of T cell-associated gene expression and acquisition of natural killer (NK) cell-like properties. These results give important insights into differentiation of murine and human lymphoid progenitors driven by synthetic CAR transgene-expression and inform the potential use of ex vivo generated CARiK cells as a broadly applicable product for targeted immunotherapy.

Publication Title

Chimeric antigen receptor-induced BCL11B suppression propagates NK-like cell development.

Sample Metadata Fields

Specimen part, Cell line

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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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