To evaluate gene expression profiles on different dendritic cell subsets isolated from spleens of mice
CD28 Deficiency Enhances Type I IFN Production by Murine Plasmacytoid Dendritic Cells.
Sex
View SamplesDifferent osteoprogenitors (SSC, BCSP, Thy+) were sorted after 2 days of JUN induction, followed by RNA extraction and microarray analysis
Expansion of Bone Precursors through Jun as a Novel Treatment for Osteoporosis-Associated Fractures.
Specimen part
View SamplesTo probe the tissue source (cancer cell VS stromal cell) of gene expression in the mixed tumor samples, we took advantage of a set of Urothelial Cancer patient-derived xenograft (PDX) models given that the transcriptome in these models is a mixture of human RNA (derived from cancer cells) and mouse RNA (derived from stromal cells). Overall design: The cohort includes 5 different patient-derived PDX models, 3 replicates for each model, and thus a total of 15 samples
EMT- and stroma-related gene expression and resistance to PD-1 blockade in urothelial cancer.
Subject
View SamplesCurrent pipelines used to map genetrap insertion sites are based on inverse- or splinkerette-PCR methods, which despite their efficacy are prone to artifacts and do not provide information on the impact of the genetrap on the expression of the targeted gene. We developed a new method, which we named TrapSeq, for the mapping of genetrap insertions based on paired-end RNA sequencing. By recognizing chimeric mRNAs containing genetrap sequences spliced to an endogenous exon, our method identifies insertions that lead to productive trapping. Overall design: We conducted two independent screenings for sensitivity against 6-thioguanine (6TG) and an ATR inhibitor (ATRi). We applied our RNAseq-based pipeline (TrapSeq) to identify mutations that provide resistance to these reagents. Importantly, and besides its use for screenings, when applied to individual clones our method provides a fast and cost-effective way that not only identifies the insertion site of the genetrap but also reveals the impact of the insertion on the expression of the trapped gene. Please note that HAP1, haploid for all chromosomes, derives from near-haploid KBM7 parent line which was in turn obtained from a chronic myeloid leukemia patient in blast crisis phase (Carette et al. Nature 477:340-343, 2011).
Trap<sup>Seq</sup>: An RNA Sequencing-Based Pipeline for the Identification of Gene-Trap Insertions in Mammalian Cells.
Specimen part, Cell line, Subject
View SamplesThe 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.
Characterization of genetic loss-of-function of Fus in zebrafish.
No sample metadata fields
View SamplesWe performed a microarray experiment to assess the global changes in transcription occurring in leaves and roots of the vitamin B6 deficient pdx1.3 knockout mutant in comparison to WT. Vitamin B6 (pyridoxal 5-phosphate) is an essential cofactor of many metabolic enzymes. Plants biosynthesize the vitamin de novo employing two enzymes, pyridoxine synthase1 (PDX1) and PDX2. In Arabidopsis (Arabidopsis thaliana), there are two catalytically active paralogs of PDX1 (PDX1.1 and PDX1.3) producing the vitamin at comparable rates. Since single mutants are viable but the pdx1.1 pdx1.3 double mutant is lethal, the corresponding enzymes seem redundant.
Consequences of a deficit in vitamin B6 biosynthesis de novo for hormone homeostasis and root development in Arabidopsis.
Specimen part
View SamplesGrowth of the drosophila eye imaginal discs is controlled by the activation of Notch in the dorsal-ventral boundary. Overexpression in the eye disc of the Notch ligand Delta together with lola and pipsqueak from the GS(2)88A8 line induces tumoral growth. We used microarray to analyze the expression profile of tumoral discs.
Imaginal discs secrete insulin-like peptide 8 to mediate plasticity of growth and maturation.
No sample metadata fields
View SamplesGene expression studies comparing IFNg+ Tregs versus IFNg- Tregs from human peripheral blood
AKT isoforms modulate Th1-like Treg generation and function in human autoimmune disease.
Specimen part
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Identification of human germinal center light and dark zone cells and their relationship to human B-cell lymphomas.
Specimen part
View SamplesFirst experiment: Cells were cultured in sulfur amino acid-free DMEM supplemented with 0.1 mM methionine + 0.1 mM cysteine (complete) or supplemented only with 0.1 mM methionine (cysteine-free). Cells were cultured in either medium for 42 h (Long + Cys; Long -Cys) or in cysteine-free medium for 36 h followed by 6 h in complete medium (Short +Cys)
HepG2/C3A cells respond to cysteine deprivation by induction of the amino acid deprivation/integrated stress response pathway.
No sample metadata fields
View Samples