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accession-icon GSE19961
Gene Expression Profile in kidneys from Cldn16 +/+, +/-, -/- female mice
  • organism-icon Mus musculus
  • sample-icon 11 Downloadable Samples
  • Technology Badge IconIllumina MouseWG-6 v2.0 expression beadchip

Description

Claudin-16 deficiency leads to renal salt wasting in humans and mice. Analysis of renal gene expression in Claudin-16 deficient mice, compared to heterozygous and wild type littermates, was performed to gain insights into molecular mechanisms compensating salt loss. Our results indicate the upregulation of known and putative genes for renal transcellular transporters. Furthermore, we could identify a transcript so far not associated with renal salt metabolism, which will provide a first link to a human electrolyte disorder disease.

Publication Title

Targeted deletion of murine Cldn16 identifies extra- and intrarenal compensatory mechanisms of Ca2+ and Mg2+ wasting.

Sample Metadata Fields

Sex, Specimen part

View Samples
accession-icon GSE56168
Plasmid-free Chlamydia trachomatis elicit lowered inflammation, delayed apoptosis, and reduced chemoattractant expression in HeLa cells compared to plasmid-containing wild type
  • organism-icon Homo sapiens
  • sample-icon 66 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Chlamydia trachomatis serovariants are responsible for either Trachoma, the leading cause of infectious blindness or sexually transmitted disease, wherein the endocervix is the most frequently infected site in women. Disease caused by Chlamydia typically involves chronic inflammation and scarring. Recent work with a live-attenuated A2497 plasmid deficient vaccine strain (A2497-) demonstrated protection in nonhuman primates against trachoma and a lack of measurable ocular pathology in A2497- infected monkeys. We therefore performed host cell transcriptome analysis of Hela cells infected with A2497 plasmid-containing (A2497) and A2497- Chlamydia over time. Our results indicate that relative to wild type A2497, the A2497- variant illicits a transcriptome response indicative of lowered inflammation response a delayed apoptosis response, a reduction in immune cell recruitement cytokine expression and a reduction in genes involved in cell proliferation and or fibrosis-like activities. The data provided here suggests a model that may explain how plasmid deficient chlamydia may provide an immuno-protective response without the pathology normally seen with plasmid-containing bacteria.

Publication Title

Transcriptional profiling of human epithelial cells infected with plasmid-bearing and plasmid-deficient Chlamydia trachomatis.

Sample Metadata Fields

Disease, Cell line

View Samples
accession-icon GSE46227
Developmental equivalence of epiblast stem cells (EpiSCs)
  • organism-icon Mus musculus
  • sample-icon 112 Downloadable Samples
  • Technology Badge IconIllumina MouseWG-6 v2.0 expression beadchip

Description

Epiblast stem cells (EpiSCs) were derived from the epiblast or the ectoderm (epi/ect) of pre-gastrula stage to late-bud stage mouse embryos. To identify if the EpiSCs retain any original stage specific characteristics or which developmental stage of epi/ect they most closely related to, we performed microarray analysis to compare the gene expression profile of multiple EpiSC lines with that of epi/ect of 7 different stages.

Publication Title

The transcriptional and functional properties of mouse epiblast stem cells resemble the anterior primitive streak.

Sample Metadata Fields

Specimen part

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accession-icon GSE37025
Interleukin-1 receptor antagonist for recent-onset type 1 diabeties mellitus: a multicenter randomized, placebo-controlled trial
  • organism-icon Homo sapiens
  • sample-icon 228 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Background: Blocking the action of the pro-inflammatory cytokine interleukin-1 (IL-1) reduces beta-cell secretory dysfunction and apoptosis in vitro, diabetes incidence in animal models of Type 1 diabetes mellitus (T1D), and glycaemia via improved beta-cell function in patients with T2D. We hypothesised that anakinra, a recombinant human IL-1 receptor antagonist, improves beta-cell function in patients with new-onset T1D. Methods: In an individually randomised, two-group parallel trial involving 14 European tertiary referral centers, 69 patients aged 18-35 with T1D, < 12 weeks of symptoms, and standard mixed meal test (MMT) stimulated C-peptide 200 pM were enrolled between January, 2009 and July, 2011 and assigned by centralised computer-generated blocked randomisation with locked computer-file concealment to treatment with 100 mg anakinra (n=35) subcutaneously once daily or placebo (n=34) for 9 months as add-on to conventional therapy. Participants and care-givers, but not data monitoring unit, were masked to group assignment. The primary end-point was change in the two-hour area-under-the-curve C-peptide response to MMT, and secondary end-points changes in insulin requirements, glycaemia, and inflammatory markers at one, three, six, and nine months. Findings: The study was prematurely terminated due to slow accrual and is closed to follow-up. No interim analysis was performed. Ten patients withdrew in the anakinra and eight in the placebo arm, leaving 25 and 26 patients to be analysed, respectively. There was no statistical difference in adverse event category reporting between arms. Interpretation: Anakinra-treatment in T1D was safe, but the trial failed to meet primary and secondary outcome measures.

Publication Title

Interleukin-1 antagonism moderates the inflammatory state associated with Type 1 diabetes during clinical trials conducted at disease onset.

Sample Metadata Fields

Subject, Time

View Samples
accession-icon GSE68049
Canakinumab treatment for recent-onset type 1 diabeties mellitus: a multicenter randomized, placebo-controlled trial
  • organism-icon Homo sapiens
  • sample-icon 187 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Background: Blocking the action of the pro-inflammatory cytokine interleukin-1 (IL-1) reduces beta-cell secretory dysfunction and apoptosis in vitro, diabetes incidence in animal models of Type 1 diabetes mellitus (T1D), and glycaemia via improved beta-cell function in patients with T2D. We hypothesised that canakinumab, a monoclonal antibody to IL-1B, improves beta-cell function in patients with new-onset T1D. Methods: In an individually randomised, two-group parallel trial involving 12 sites in US, 69 patients aged 6-45 with T1D, < 12 weeks of symptoms, and assigned by centralised computer-generated blocked randomisation with locked computer-file concealment to treatment with 2 mg/kg (maximum 300 mg) canakinumab (n=45) or placebo (n=22) monthly for 12 months as add-on to conventional therapy. Participants and care-givers, but not data monitoring unit, were masked to group assignment. The primary end-point was change in the two-hour area-under-the-curve C-peptide response to MMT 12 months.

Publication Title

Interleukin-1 antagonism moderates the inflammatory state associated with Type 1 diabetes during clinical trials conducted at disease onset.

Sample Metadata Fields

Subject, Time

View Samples
accession-icon GSE8194
Cis-transcriptional variation in maize inbred lines B73 and Mo17 leads to additive expression
  • organism-icon Zea mays
  • sample-icon 36 Downloadable Samples
  • Technology Badge Icon Affymetrix Maize Genome Array (maize)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Cis-transcriptional variation in maize inbred lines B73 and Mo17 leads to additive expression patterns in the F1 hybrid.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon GSE35427
Transcriptional response to soybean aphid infestation in susceptible and resistant soybean plants
  • organism-icon Glycine max
  • sample-icon 22 Downloadable Samples
  • Technology Badge Icon Affymetrix Soybean Genome Array (soybean)

Description

Soybean aphids are phloem-feeding pests that can cause significant yield losses in soybean plants. Soybean aphids thrive on susceptible soybean lines but not on resistant lines.

Publication Title

Multiple phytohormone signals control the transcriptional response to soybean aphid infestation in susceptible and resistant soybean plants.

Sample Metadata Fields

Specimen part

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accession-icon GSE8174
Cis-transcriptional variation in maize inbred lines B73 and Mo17 leads to additive expression - Seedling data
  • organism-icon Zea mays
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Maize Genome Array (maize)

Description

Microarray analysis of gene expression patterns in immature ear, seedling, and embryo tissues from the maize inbred lines B73 and Mo17 identified numerous genes with variable expression. Some genes had detectable expression in only one of the two inbreds; most of these genes were detected in the genomic DNA of both inbreds, indicating that the expression differences are likely caused by differential regulation rather than by differences in gene content. Gene expression was also monitored in the reciprocal F1 hybrids B73xMo17 and Mo17xB73. The reciprocal F1 hybrid lines did not display parental effects on gene expression levels. Approximately 80% of the differentially expressed genes displayed additive expression patterns in the hybrids relative to the inbred parents. The approximately 20% of genes that display nonadditive expression patterns tend to be expressed at levels within the parental range, with minimal evidence for novel expression levels greater than the high parent or less than the low parent. Analysis of allele-specific expression patterns in the hybrid suggested that intraspecific variation in gene expression levels is largely attributable to cis-regulatory variation in maize. Collectively, our data suggest that allelic cis-regulatory variation between B73 and Mo17 dictates maintenance of inbred allelic expression levels in the F1 hybrid, resulting in additive expression patterns.

Publication Title

Cis-transcriptional variation in maize inbred lines B73 and Mo17 leads to additive expression patterns in the F1 hybrid.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon GSE8179
Cis-transcriptional variation in maize inbred lines B73 and Mo17 leads to additive expression - Embryo data
  • organism-icon Zea mays
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Maize Genome Array (maize)

Description

Microarray analysis of gene expression patterns in immature ear, seedling, and embryo tissues from the maize inbred lines B73 and Mo17 identified numerous genes with variable expression. Some genes had detectable expression in only one of the two inbreds; most of these genes were detected in the genomic DNA of both inbreds, indicating that the expression differences are likely caused by differential regulation rather than by differences in gene content. Gene expression was also monitored in the reciprocal F1 hybrids B73xMo17 and Mo17xB73. The reciprocal F1 hybrid lines did not display parental effects on gene expression levels. Approximately 80% of the differentially expressed genes displayed additive expression patterns in the hybrids relative to the inbred parents. The approximately 20% of genes that display nonadditive expression patterns tend to be expressed at levels within the parental range, with minimal evidence for novel expression levels greater than the high parent or less than the low parent. Analysis of allele-specific expression patterns in the hybrid suggested that intraspecific variation in gene expression levels is largely attributable to cis-regulatory variation in maize. Collectively, our data suggest that allelic cis-regulatory variation between B73 and Mo17 dictates maintenance of inbred allelic expression levels in the F1 hybrid, resulting in additive expression patterns.

Publication Title

Cis-transcriptional variation in maize inbred lines B73 and Mo17 leads to additive expression patterns in the F1 hybrid.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon GSE8176
Cis-transcriptional variation in maize inbred lines B73 and Mo17 leads to additive expression - Immature ear data
  • organism-icon Zea mays
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Maize Genome Array (maize)

Description

Microarray analysis of gene expression patterns in immature ear, seedling, and embryo tissues from the maize inbred lines B73 and Mo17 identified numerous genes with variable expression. Some genes had detectable expression in only one of the two inbreds; most of these genes were detected in the genomic DNA of both inbreds, indicating that the expression differences are likely caused by differential regulation rather than by differences in gene content. Gene expression was also monitored in the reciprocal F1 hybrids B73xMo17 and Mo17xB73. The reciprocal F1 hybrid lines did not display parental effects on gene expression levels. Approximately 80% of the differentially expressed genes displayed additive expression patterns in the hybrids relative to the inbred parents. The approximately 20% of genes that display nonadditive expression patterns tend to be expressed at levels within the parental range, with minimal evidence for novel expression levels greater than the high parent or less than the low parent. Analysis of allele-specific expression patterns in the hybrid suggested that intraspecific variation in gene expression levels is largely attributable to cis-regulatory variation in maize. Collectively, our data suggest that allelic cis-regulatory variation between B73 and Mo17 dictates maintenance of inbred allelic expression levels in the F1 hybrid, resulting in additive expression patterns.

Publication Title

Cis-transcriptional variation in maize inbred lines B73 and Mo17 leads to additive expression patterns in the F1 hybrid.

Sample Metadata Fields

No sample metadata fields

View Samples
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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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