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accession-icon GSE6055
Gene Expression Profiling Reveals Unique Pathways Associated with Differential Severity of Lyme Arthritis
  • organism-icon Mus musculus
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Expression 430A Array (moe430a)

Description

The murine model of Lyme disease provides a unique opportunity to study the localized host response to similar stimulus, B. burgdorferi, in the joints of mice destined to develop severe arthritis (C3H) or mild disease (C57BL/6). Pathways associated with the response to infection and the development of Lyme arthritis were identified by global gene expression patterns using oligonucleotide microarrays. A robust induction of IFN responsive genes was observed in severely arthritic C3H mice at one week of infection, which was absent from mildly arthritic C57BL/6 mice. In contrast, infected C57BL/6 mice displayed a novel expression profile characterized by genes involved in epidermal differentiation and wound repair, which were decreased in the joints of C3H mice. These expression patterns were associated with disease state rather than inherent differences between C3H and C57BL/6 mice, as C57BL/6-IL10-/- mice infected with B. burgdorferi develop more severe arthritis that C57BL/6 mice and displayed an early gene expression profile similar to C3H mice. Gene expression profiles at two and four weeks post infection revealed a common response of all strains that was likely to be important for the host defense to B. burgdorferi and mediated by NF-kB-dependent signaling. The gene expression profiles identified in this study add to the current understanding of the host response to B. burgdorferi and identify two novel pathways that may be involved in regulating the severity of Lyme arthritis.

Publication Title

Gene expression profiling reveals unique pathways associated with differential severity of lyme arthritis.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE16195
Expression profiling of joint tissue from C3H and interval specific congenic mouse lines post- B. burgdorferi infection
  • organism-icon Mus musculus
  • sample-icon 10 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Gene expression profile of joint tissue from C3H and interval specific congenic mouse lines (ISCL) following infection with Borrelia burgdorferi

Publication Title

Interval-specific congenic lines reveal quantitative trait Loci with penetrant lyme arthritis phenotypes on chromosomes 5, 11, and 12.

Sample Metadata Fields

Specimen part

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accession-icon SRP101281
Programed cell removal of Neutrophils regulated by calreticulin
  • organism-icon Mus musculus
  • sample-icon 12 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

RNA seq analysis for pathwayidentification to identify Overall design: RNA Seq analysis of apoptotic resistant and WT neutrophils isolated from bone marrow and peritoneum after thiglycollate induced inflammation

Publication Title

Programmed cell removal by calreticulin in tissue homeostasis and cancer.

Sample Metadata Fields

Specimen part, Cell line, Subject

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accession-icon GSE49516
Long Intergenic Non-Coding RNA HOTAIRM1 Regulates Cell Cycle Progression During Myeloid Maturation in NB4 Promyelocytic Leukemia Cells
  • organism-icon Homo sapiens
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

HOTAIRM1 is a long intergenic non-coding RNA located in the human HOXA gene cluster, with gene expression highly specific for maturing myeloid cells, particularly during all-trans retinoic acid (ATRA) induction of granolopoiesis in NB4, a human t(15;17) acute promyelocytic leukemia (APL) cell line. We sought to assess the impact of HOTAIR knockdown on the global programme of gene expression underlying the granulocytic maturing process in NB4 cells.

Publication Title

Long intergenic non-coding RNA HOTAIRM1 regulates cell cycle progression during myeloid maturation in NB4 human promyelocytic leukemia cells.

Sample Metadata Fields

Specimen part, Cell line, Treatment

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accession-icon GSE38461
Expression data from clone sorted tumor endothelial subsets
  • organism-icon Mus musculus
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Competitive interactions between emerging blood vessels determine the clonogenic contribution to developing vascualture. Using a multi-color cre reporter, CD31+CD45-VeCad+ clones were isolated and analyzed for expression differences.

Publication Title

Dynamic Patterns of Clonal Evolution in Tumor Vasculature Underlie Alterations in Lymphocyte-Endothelial Recognition to Foster Tumor Immune Escape.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE3541
DNA microarray reveals novel genes induced by mechanical forces in fetal lung type II epithelial cells
  • organism-icon Rattus norvegicus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Rat Expression 230A Array (rae230a)

Description

Mechanical forces are essential for normal fetal lung development. However, the cellular and molecular mechanisms regulating this process remain largely unknown. In the present study, we used oligonucleotide microarray technology to investigate gene expression profile in cultured E19 rat fetal lung type II epithelial cells exposed to a level of mechanical strain similar to that observed in utero. Significance Analysis of Microarrays (SAM) identified 92 genes differentially expressed by strain. Interestingly, several members of the solute carrier family of amino acid transporters, genes involved in amino acid synthesis and development, and amiloride-sensitive epithelial sodium channel gene were induced by strain. These results were confirmed by quantitative real-time polymerase chain reaction (qRT-PCR). Thus, this study identifies genes induced by strain that may be important for amino acid signaling pathways, protein synthesis and development in fetal type II cells. In addition, these data suggest that mechanical forces may contribute to facilitate lung fluid reabsorption in preparation for birth. Taken together, the present investigation provides further insights into how mechanical forces may modulate fetal lung development.

Publication Title

DNA microarray reveals novel genes induced by mechanical forces in fetal lung type II epithelial cells.

Sample Metadata Fields

Sex, Specimen part

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accession-icon SRP002605
Analysis of HeLa cells after transfection with miR-1 or miR-155, by ribosome profiling and mRNA-Seq
  • organism-icon Homo sapiens
  • sample-icon 24 Downloadable Samples
  • Technology Badge IconIlluminaGenomeAnalyzerII

Description

MicroRNAs (miRNAs) are endogenous ~22-nucleotide RNAs that mediate important gene-regulatory events by pairing to the mRNAs of protein-coding genes to direct their repression. Repression of these regulatory targets leads to decreased translational efficiency and/or decreased mRNA levels, but the relative contributions of these two outcomes have been largely unknown, particularly for endogenous targets expressed at low-to-moderate levels. Here, we use ribosome profiling to measure the overall effects on protein production and compare these to simultaneously measured effects on mRNA levels. For both ectopic and endogenous miRNA regulatory interactions, lowered mRNA levels account for most (=84%) of the decreased protein production. These results show that changes in mRNA levels closely reflect the impact of miRNAs on gene expression and indicate that destabilization of target mRNAs is the predominant reason for reduced protein output. Overall design: Examine ribosome footprints and mRNA abundance of HeLa cells transfected with miR-1 or miR-155, versus mock-transfected cells, at two different time points post-transfection. Supplementary processed data files linked below. mir155_summaryTable.txt: log2 fold changes (miR-155-transfected versus mock-transfected HeLa cells, 32hr). mir1_summaryTable.txt: log2 fold changes (miR-1-transfected versus mock-transfected HeLa cells, 32hr).

Publication Title

Mammalian microRNAs predominantly act to decrease target mRNA levels.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE22004
Mammalian microRNAs predominantly act to decrease target mRNA levels
  • organism-icon Mus musculus, Homo sapiens
  • sample-icon 8 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2), Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

MicroRNAs (miRNAs) are endogenous ~22-nucleotide RNAs that mediate important gene-regulatory events by pairing to the mRNAs of protein-coding genes to direct their repression. Repression of these regulatory targets leads to decreased translational efficiency and/or decreased mRNA levels, but the relative contributions of these two outcomes have been largely unknown, particularly for endogenous targets expressed at low-to-moderate levels. Here, we use ribosome profiling to measure the overall effects on protein production and compare these to simultaneously measured effects on mRNA levels. For both ectopic and endogenous miRNA regulatory interactions, lowered mRNA levels account for most (84%) of the decreased protein production. These results show that changes in mRNA levels closely reflect the impact of miRNAs on gene expression and indicate that destabilization of target mRNAs is the predominant reason for reduced protein output.

Publication Title

Mammalian microRNAs predominantly act to decrease target mRNA levels.

Sample Metadata Fields

Time

View Samples
accession-icon SRP065478
Snai2 and Snai3 transcriptionally regulate cellular fitness and functionality of T cell lineages through distinct gene programs
  • organism-icon Mus musculus
  • sample-icon 23 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

T lymphocytes are essential contributors to the adaptive immune system and consist of multiple lineages that serve various effector and regulatory roles. As such, precise control of gene expression is essential to the proper development and function of these cells. Previously, we identified Snai2 and Snai3 as being essential regulators of immune tolerance partly due to the impaired function of CD4+ regulatory T cells in Snai2/3 conditional double knockout mice. Here we extend those previous findings using a bone marrow transplantation model to provide an environmentally unbiased view of the molecular changes imparted onto various T lymphocyte populations once Snai2 and Snai3 are deleted. The data presented here demonstrate that Snai2 and Snai3 transcriptionally regulate the cellular fitness and functionality of not only CD4+ regulatory T cells but effector CD8a+ and CD4+ conventional T cells as well. This is achieved through the modulation of gene sets unique to each cell type and includes transcriptional targets relevant to the survival and function of each T cell lineage. As such, Snai2 and Snai3 are essential regulators of T cell immunobiology. Overall design: GFP- CD3e+ CD8a+ CD4-, GFP- CD3e+ CD8a- CD4+ CD25- and GFP- CD3e+ CD8a- CD4+ CD25+ T cells were isolated from spleens of UBC-GFP mice transplanted with WT or cDKO lineage-depleted donor bone marrow following lethal irradiation of recipient mice. RNA-seq was performed on 3-4 biological replicates from each genotype for all T cell populations analyzed.

Publication Title

Snai2 and Snai3 transcriptionally regulate cellular fitness and functionality of T cell lineages through distinct gene programs.

Sample Metadata Fields

Specimen part, Cell line, Subject

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accession-icon SRP038992
Ribosomal footprinting and RNASeq in two strains of yeast and their diploid hybrid
  • organism-icon Saccharomyces cerevisiae
  • sample-icon 8 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

Heritable differences in gene expression between individuals are an important source of phenotypic variation. The question of how closely the effects of genetic variation on protein levels mirror those on mRNA levels remains open. Here, we addressed this question by using ribosomal footprinting to examine how genetic differences between two strains of the yeast S. cerevisiae affect translation. Strain differences in translation were observed for hundreds of genes, more than half as many as showed genetic differences in mRNA levels. Similarly, allele specific measurements in the diploid hybrid between the two strains found roughly half as many cis-acting effects on translation as were observed for mRNA levels. In both the parents and the hybrid, strong effects on translation were rare, such that the direction of an mRNA difference was typically reflected in a concordant footprint difference. The relative importance of cis and trans acting variation on footprint levels was similar to that for mRNA levels. Across all expressed genes, there was a tendency for translation to more often reinforce than buffer mRNA differences, resulting in footprint differences with greater magnitudes than the mRNA differences. Finally, we catalogued instances of premature translation termination in the two yeast strains. Overall, genetic variation clearly influences translation, but primarily does so by subtly modulating differences in mRNA levels. Translation does not appear to create strong discrepancies between genetic influences on mRNA and protein levels. Overall design: Ribsosomal footprinting and RNASeq in the two yeast strains BY and RM as well as their diploid hybrid. We generated one library each for the BY and RM parents, and two libraries (biological replicates) for the hybrid data.

Publication Title

Genetic influences on translation in yeast.

Sample Metadata Fields

Cell line, Subject

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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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