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GSE9239
Homo sapiens
6 Downloadable Samples
Affymetrix Human Genome U133A 2.0 Array (hgu133a2)
Description
The process for making monocyte derived DCs (moDCs) has been previously described (46). All analysis was performed on day 5 immature DCs. Etanercept 10mg/mL was added to experimental wells on days 0, 2, and 4. We chose this concentration of etanercept as it approximates the plasma concentration of drug when given 50mg BIW.
Publication Title
Amelioration of epidermal hyperplasia by TNF inhibition is associated with reduced Th17 responses.
Sample Metadata Fields
No sample metadata fields
View Samples- Homo sapiens
- 14 Downloadable Samples
- Affymetrix Human Genome U133A 2.0 Array (hgu133a2)
Description
To understand the development of new psoriasis lesions, we studied a group of moderate-to-severe psoriasis patients who experienced a relapse after ceasing efalizumab (anti-CD11a, Raptiva, Genentech). There were increased CD3+ T cells, neutrophils, CD11c+ and CD83+ myeloid DCs, but no increase in CD1c+ resident myeloid DCs. In relapsed lesions, there were many CD11c+CD1c-, inflammatory myeloid DCs identified by TNFSF10/TRAIL, TNF, and iNOS. CD11c+ cells in relapsed lesions co-expressed CD14 and CD16 in situ. Efalizumab induced an improvement in many psoriasis genes, and during relapse, the majority of these genes reversed back to a lesional state. Gene Set Enrichment Analysis (GSEA) of the transcriptome of relapsed tissue showed that many of the gene sets known to be present in psoriasis were also highly enriched in relapse. Hence, on ceasing efalizumab, T cells and myeloid cells rapidly enter the skin to cause classic psoriasis.
Publication Title
Post-therapeutic relapse of psoriasis after CD11a blockade is associated with T cells and inflammatory myeloid DCs.
Sample Metadata Fields
Specimen part, Disease, Disease stage, Treatment, Subject, Time
View Samples- Homo sapiens
- 12 Downloadable Samples
- Affymetrix Human Genome U133A 2.0 Array (hgu133a2)
Description
In this study, we shought to identify the cytokines produced by skin-resident T cells in normal skin, localize the receptors for these cytokines, and examine how these cytokines alter gene expression profiles of the cells bearing cognate receptors.
Publication Title
Th17 cytokines interleukin (IL)-17 and IL-22 modulate distinct inflammatory and keratinocyte-response pathways.
Sample Metadata Fields
No sample metadata fields
View Samples- Bos taurus
- 6 Downloadable Samples
- Affymetrix Bovine Genome Array (bovine)
Description
Using microarrays, genome-wide RNA expression was profiled and compared for in vitro fertilization (IVF) - derived blastocysts and embryos undergoing degenerative development up to the same time point. Surprisingly similar transcriptomic profiles were found in degenerative embryos and blastocysts. Nonetheless, we identified 67 transcripts that significantly differed between these two groups of embryos at a 15% false discovery rate, including 33 transcripts showing at least a two-fold difference. Several signaling and metabolic pathways were found to be associated with the developmental status of embryos, among which were previously known important steroid biosynthesis and cell communication pathways in early embryonic development.
Publication Title
Transcriptomic profiling of bovine IVF embryos revealed candidate genes and pathways involved in early embryonic development.
Sample Metadata Fields
Specimen part
View Samples- Homo sapiens
- 6 Downloadable Samples
NextSeq 500
Description
We performed a 3' RACE of a novel HIV RNA TAR-gag in order to determine the sequence of the RNA at the 3' end. Our data had shown that TAR-gag was potentially a noncoding RNA and our hypothesis was that TAR-gag ended somewhere prior to the end of the gag region of the HIV genome. The 3' RACE experiment showed that TAR-gag actually consists of four different RNA clusters, the longest of which ends at 615 bases from the transcription start site; this is in the middle of the p17 region of the gag gene. In addition, we sequenced all host RNAs in the EVs. Overall design: RNA from J1.1 and U1 exosomes was isolated and converted to cDNA. Sequencing libraries of the cDNA were made and a 3' RACE was perforemed to determine how long TAR-gag RNA is. Please note that the clustering analysis (published in PMID 28536264) was done only on the unfragmented samples (i.e. *-U samples).
Publication Title
An Omics Approach to Extracellular Vesicles from HIV-1 Infected Cells.
Sample Metadata Fields
Specimen part, Subject
View Samples- Homo sapiens
- 272 Downloadable Samples
- Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
This dataset is composed of the unique patients (276; at the Day 1 timepoint) that are present in the six other GEO datasets published by Hector Wong and the Genomics of Pediatric SIRS and Septic Shock Investigators. This dataset thus includes all unique patients from GSE4607, GSE8121, GSE9692, GSE13904, GSE26378, and GSE26440. These are only from the Day 1 timepoint.
Publication Title
A comprehensive time-course-based multicohort analysis of sepsis and sterile inflammation reveals a robust diagnostic gene set.
Sample Metadata Fields
Specimen part, Disease
View Samples- Bos taurus
- 2 Downloadable Samples
- Illumina HiSeq 2000
Description
Transcriptome of CDKN1C-siRNA-injected embryos were compared to sham-injected embryos using RNA-sequencing to determine the genes and pathways downstream of the silenced gene that may have been altered. Overall design: Transcriptome comparison between two pools of embryos (i.e. CDKN1C-siRNA-injected vs sham-injected embryos)
Publication Title
Knockdown of CDKN1C (p57(kip2)) and PHLDA2 results in developmental changes in bovine pre-implantation embryos.
Sample Metadata Fields
Specimen part, Subject
View Samples- Homo sapiens
- 60 Downloadable Samples
- Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
This study provides a comprehensive evaluation of changes in gene expression during treatment with Genistein in vitro.
Publication Title
Dose- and Time-Dependent Transcriptional Response of Ishikawa Cells Exposed to Genistein.
Sample Metadata Fields
Treatment
View Samples- Homo sapiens
- 24 Downloadable Samples
- IlluminaHiSeq2000
Description
FOXE3 is a lens specific transcription factor that has been associated with anterior segment ocular dysgenesis. To determine the transcriptional target(s) of FOXE3 that are indispensable for the anterior segment development, we examined the transcriptome and the proteome of cells expressing truncated FOXE3 responsible for Peters anomaly identified through linkage-coupled next-generation whole exome sequencing. We found that DNAJB1, an autophagy-associated protein, was the only candidate exhibiting differential expression in both screens. We confirmed the candidacy of DNAJB1 through chromatin immunoprecipitation and luciferase assays while knockdown of DNAJB1 in human lens epithelial cells resulted in mitotic arrest. Subsequently, we targeted dnajb1a in zebrafish through injection of a splice-blocking morpholino. The dnajb1a morphants exhibited underdeveloped cataractous lenses with persistent apoptotic nuclei. In conclusion, we have identified DNAJB1 as a transcriptional target of FOXE3 in a novel pathway that is crucial for development of the anterior segment of the eye. Overall design: Human Embryonic Kidney (HEK293FT) cells were transfected with the expression vector (pT-RexTM-DEST30) harboring either the wild type or the mutant (C240*) FOXE3 ORF (open reading frame). The experimental design included a total of eight biological replicates of cells expressing the wild type and eight replicates of mutant FOXE3 along with eight non-transfected controls. Cells were harvested 24-hour post-transfection and subjected to total RNA isolation for the preparation of whole transcriptome next-generation sequencing libraries. Initially, we examined the quality of transcriptome libraries on a MiSeq genome analyzer. Subsequent to confirmation of the quality, all libraries were paired-end sequenced (2 x 100 bp) using Illumina TruSeq Cluster V3 flow cell at a concentration of 13.0 pM in two separate lanes (12 bar-coded mRNA pooled libraries in each lane) on a HiSeq 2000 genome analyzer.
Publication Title
FOXE3 contributes to Peters anomaly through transcriptional regulation of an autophagy-associated protein termed DNAJB1.
Sample Metadata Fields
No sample metadata fields
View Samples- Homo sapiens
- 119 Downloadable Samples
- Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
CONTEXT Slowly progressive chronic tubulo-interstitial damage jeopardizes long-term renal allograft survival. Both immune and non-immune mechanisms are thought to contribute, but the most promising targets for timely intervention have not been identified. OBJECTIVE In the current study we seek to determine the driving force behind progressive histological damage of renal allografts, without the interference of donor pathology, delayed graft function and acute graft rejection. DESIGN We used microarrays to examine whole genome expression profiles in renal allograft protocol biopsies, and analyzed the correlation between gene expression and the histological appearance over time. The gene expression profiles in these protocol biopsies were then compared with gene expression of biopsies with acute T-cell mediated rejection. PATIENTS Human renal allograft biopsies (N=120) were included: 96 rejection-free protocol biopsies and 24 biopsies with T-cell mediated acute rejection. RESULTS In this highly cross-validated study, we demonstrate the significant association of established, ongoing and future chronic histological damage with regulation of adaptive immune gene expression (T-cell and B-cell transcript sets) and innate immune response gene expression (dendritic cell, NK-cell, mast cell and granulocyte transcripts). We demonstrate the ability of gene expression analysis to perform as a quantitative marker for ongoing inflammation with a wide dynamic range: from subtle subhistological inflammation prior to development of chronic damage, over moderate subclinical inflammation associated with chronic histological damage, to marked inflammation of Banff-grade acute T-cell mediated rejection. CONCLUSION Progressive chronic histological damage after kidney transplantation is associated with significant regulation of both innate and adaptive immune responses, months before the histological lesions appear. This study therefore corroborates the hypothesis that quantitative inflammation below the diagnostic threshold of classic T-cell or antibody-mediated rejection is associated with early subclinical stages of progressive renal allograft damage.
Publication Title
Progressive histological damage in renal allografts is associated with expression of innate and adaptive immunity genes.
Sample Metadata Fields
Specimen part, Time
View Samples