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SRP167958
Mus musculus
4 Downloadable Samples
NextSeq 500
Description
We performed total RNA-Seq of murine Th1 cells which were four times reactivated in vitro in the presence of irradiated APC'srepeatedly activated in vitro. Overall design: CD4+CD62Lhi (naive) cells were isolated from C57BL/6 mice, activated with aCD3 and aCD28 an cultured under Th1 polarizing conditions in the presence of irradiated APCs. Every sixth day cells were harvested, restimulated with aCD3 and aCD28 and cultured under Th1 polarizing conditions in the presence of irradiated APCs APCs. After four rounds of restimulation, total RNA was extracted and cDNA libraries for total RNA sequencing were generated using “TruSeq® Stranded Total RNA Library” kit (Illumina, San Diego, CA, USA).
Publication Title
MicroRNA-31 Reduces the Motility of Proinflammatory T Helper 1 Lymphocytes.
Sample Metadata Fields
Specimen part, Subject
View Samples- Mus musculus
- 6 Downloadable Samples
- Illumina HiSeq 2000
Description
Purpose:The goals of this study was to determine alterations in expression levels of transcripts downstream of a dominant-negative transcription factor. Quantitative reverse transcription polymerase chain reaction (qRT–PCR) methods was used to confirm the altered expression of targets. Methods: Striatal mRNA profiles of 11-month-old wild-type (WT) and Nestin-Cre X PPAR delta E411P mice were generated by deep sequencing, in triplicate, using Illumina HiSeq 2000. The sequence reads that passed quality filters were analyzed at the transcript isoform level with TopHat followed by Cufflinks. qRT–PCR validation was performed using TaqMan and SYBR Green assays. Western blots, and immunofluorescence was also used to confirm if altered mRNA levels translated to changes at the protein level. Results: Using data analysis workflow, we mapped sequence reads for each sample to the mouse genome (build mm9) and identified transcripts in the striatum of WT and PPARdelta E411P mice. Conclusions: Our study found multiple transcripts altered in the striatum of the Nestin-Cre x PPAR delta E411P mice as compared to WT striatum, as generated by RNA-SEQ in biologic replicates. Overall design: Striatal mRNA profiles of 11-month-old wild type (WT) and Nestin-Cre X PPAR delta E411P mice were generated by deep sequencing, in triplicate, using Illumina HiSeq2000.
Publication Title
PPAR-δ is repressed in Huntington's disease, is required for normal neuronal function and can be targeted therapeutically.
Sample Metadata Fields
Specimen part, Cell line, Subject
View Samples- Mus musculus, Homo sapiens
- 28 Downloadable Samples
Illumina MouseWG-6 v2.0 expression beadchip, Illumina HumanHT-12 V4.0 expression beadchip
Description
This SuperSeries is composed of the SubSeries listed below.
Publication Title
Microbiome Influences Prenatal and Adult Microglia in a Sex-Specific Manner.
Sample Metadata Fields
Sex, Specimen part
View Samples- Mus musculus
- 28 Downloadable Samples
Illumina MouseWG-6 v2.0 expression beadchip
Description
Microarray analysis of murine microglia from different stages of development was performed. Results showed that different phases of microglia development had different group of genes up-regulated for specific functions.
Publication Title
Microbiome Influences Prenatal and Adult Microglia in a Sex-Specific Manner.
Sample Metadata Fields
Specimen part
View Samples- Mus musculus
- 23 Downloadable Samples
- Illumina HiSeq 2500
Description
RNAseq was performed on microglia from male and female, SPF or GF mice to elucidate the genetic differences implicated by microbiota and gender. DEGs between the various groups gave some ideas on what different pathways or functions might be affected due to the different factors. Overall design: Microglia from SPF and GF mice from embryonic and adult stages of both gender were sorted for sequencing. DEGs were obtained to observe if any signicant genes were affected. Pathway analysis was performed with the set of DEGs.
Publication Title
Microbiome Influences Prenatal and Adult Microglia in a Sex-Specific Manner.
Sample Metadata Fields
Specimen part, Cell line, Subject
View Samples- Homo sapiens
- 15 Downloadable Samples
- Affymetrix Human Genome U133A 2.0 Array (hgu133a2)
Description
Human dendritic cells (DC) are suppressed by tumor-derived alpha fetoprotein (AFP), but less so by cord blood-derived normal AFP.
Publication Title
Tumor-derived α-fetoprotein impairs the differentiation and T cell stimulatory activity of human dendritic cells.
Sample Metadata Fields
Specimen part, Subject
View Samples- Homo sapiens
- 19 Downloadable Samples
- Illumina HiSeq 2000
Description
Objectives: The collagen VI related muscular dystrophies (COL6-RD), Ullrich congenital muscular dystrophy (UCMD) and Bethlem myopathy (BM) are among the most common congenital muscular dystrophies, but the pathogenesis, including the role of mutant collagen VI in the matrix is poorly understood. To better define the pathways disrupted by mutations in collagen VI, we have used a transcriptional profiling approach with RNA-Seq to identify differentially expressed genes in COL6-RD patients from controls. Methods: We have used RNA-Seq to identify differentially expressed genes in cultured dermal fibroblasts from 13 COL6-RD patients (8 dominant negative and 5 null) and 6 controls. Sequence reads were analyzed using the TopHat/Cufflinks pipeline. Results: Differentially expressed transcripts between COL6-RD patient and control fibroblasts include upregulation of ECM components and downregulation of factors controlling matrix remodeling and repair. DN and null samples are differentiated by downregulation of genes involved with DNA replication and repair in null samples Overall design: Expression profiles of dermal fibroblasts from 13 COL6-RD patients with dominant negative (8) or null (5) mutations compared to 6 control fibroblasts.
Publication Title
Transcriptome profiling identifies regulators of pathogenesis in collagen VI related muscular dystrophy.
Sample Metadata Fields
Specimen part, Subject
View Samples- Danio rerio
- 16 Downloadable Samples
- IlluminaHiSeq2500
Description
The RNA-binding protein FUS is implicated in transcription, alternative splicing of neuronal genes and DNA repair. Mutations in FUS have been linked to human neurodegenerative diseases such as ALS (amyotrophic lateral sclerosis). We genetically disrupted fus in zebrafish (Danio rerio) using the CRISPR-Cas9 system. The fus knockout animals are fertile and did not show any distinctive phenotype. Mutation of fus induces mild changes in gene expression on the transcriptome and proteome level in the adult brain. We observed a significant influence of genetic background on gene expression and 3’UTR usage, which could mask the effects of loss of Fus. Unlike published fus morphants, maternal zygotic fus mutants do not show motoneuronal degeneration and exhibit normal locomotor activity. Overall design: We performed paired-end sequencing (100bp reads) of the polyA+ transcriptome from brains of five individuals with Fus-/- genotype and four with Fus wild type genotype. Note on RNA-Seq replicates: after performing first RNA sequencing on four replicates of Fus-/- and WT (labeled with the prefix "Sample_imb_ketting_2014_13_") we received a notice from Illumina stating a problem with the library preparation kit lot that was used to prepare the libraries. Due to that, we performed RNA sequencing a second time, using the same input RNA, except for the Fus knockout replicate #3, because there was not enough input RNA left. Instead, a different Fus knockout replicate (#1) was sequenced. However, we compared the mapped reads from sequencing run 1 and sequencing run 2 using plotCorrelaction from DeepTools, and the samples are highly correlated (at least 0.97 and 0.95, Spearman and Pearson correlation respectively). Therefore, we considered first ("Sample_imb_ketting_2014_13_") and second sequencing runs as technical replicates.
Publication Title
Characterization of genetic loss-of-function of Fus in zebrafish.
Sample Metadata Fields
No sample metadata fields
View Samples- Homo sapiens
- 9 Downloadable Samples
- Illumina HumanHT-12 V4.0 expression beadchip
Description
Hepatocellular carcinoma (HCC) is a fatal malignancy with a dismal prognosis. The recent advances in genomics and transcriptomics have led to large volumes of molecular data for HCC, providing an unprecedented opportunity to translate these data into more effective therapeutics. By creating HCC gene expression signatures and comparing with drug response signatures from multiple datasets, we identified four antihelminthics (from over 1000 FDA-approved drugs) that can reverse the HCC disease gene expression. Among these four, niclosamide was the top hit, which we further evaluated in clinically relevant HCC cell lines and patient-derived xenografts (PDX). Given the poor water-solubility and limited systemic bioavailability of niclosamide, we also evaluated its ethanolamine salt (NEN), which has improved solubility and bioavailability. Both niclosamide and NEN significantly inhibited HCC cell proliferation in vitro, which was associated with down-regulation of key proteins involved in the AKT-mTOR, Wnt, Stat3, and EGFR/Ras/Raf signaling pathways. NEN additionally decreased the growth of three PDX models after oral administration (1,5000 ppm in food) for 4-6 weeks. Expression profiling demonstrated that niclosamide and NEN induced highly similar gene expression changes in HepG2 cells and in PDX models, and that both compounds significantly reversed HCC gene expression in vitro and in vivo . Our results suggest that NEN may be a preferred drug candidate for the treatment of HCC.
Publication Title
Computational Discovery of Niclosamide Ethanolamine, a Repurposed Drug Candidate That Reduces Growth of Hepatocellular Carcinoma Cells In Vitro and in Mice by Inhibiting Cell Division Cycle 37 Signaling.
Sample Metadata Fields
Cell line, Treatment
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