To understand the molecular mechanisms of human lung macrophage development, function, and role in BPD pathogenesis, we conducted a clinical study using isolated tracheal aspirate macrophages from intubated preterm infants born before 30 wk gestation. One hundred twenty-eight patients intubated for respiratory distress syndrome and surfactant administration were consented for the study.
Transcriptional profiling of lung macrophages identifies a predictive signature for inflammatory lung disease in preterm infants.
Sex, Treatment
View SamplesGoal was to identify yeast genes whose expression changed as a function of the shift from growth in bulk culture to growth in an air-liquid interfacial biofilm.
Ethanol-independent biofilm formation by a flor wine yeast strain of Saccharomyces cerevisiae.
Specimen part
View Samples5' selective RNA-seq of 96 single cells from human nasal epithelial cells. Cells grown for 33 days at an air liquid interface. RNAseq profiling was performed with N4H4 unique molecular identifiers processed on a Fluidigm C1. Sequencing was performed on a Ion Proton (Life Technologies). Overall design: Single cell from human nasal epithelium. 5' selective RNAseq profiling, 96 cells, unique molecular identifiers, custom library preparation.
A cost effective 5΄ selective single cell transcriptome profiling approach with improved UMI design.
Specimen part, Subject
View Samples5' selective RNA-seq of 47 Single HEK293 cells RNAseq profiling with N4H4 unique molecular identifiers processed on a Fluidigm C1. Overall design: Single cell HEK293 cell 5' selective RNAseq profiling, 47 cells, unique molecular identifiers, custom library preparation.
A cost effective 5΄ selective single cell transcriptome profiling approach with improved UMI design.
No sample metadata fields
View SamplesFive libraries from 100 HEK293 cells each were prepared using a Smartseq based custom library preparation approach with unique molecular identifiers. One batch of 2 replicates (A) and one batch of 3 replicates (B) were prepared from different cell cultures. Libraries were sequenced on an Ion Proton Overall design: HEK293 cell (100 cells) 5' selective RNAseq profiling, N4H4 unique molecular identifiers, 2 replicates (A) and 3 replicates (B)
A cost effective 5΄ selective single cell transcriptome profiling approach with improved UMI design.
No sample metadata fields
View SamplesComparison of gene expression profiles from C. elegans wildtype strain (N2) treated with L4440 and T25B9.1 RNAi for 5 days after L4 larvae stage. Jena Centre for Systems Biology of Ageing - JenAge (ww.jenage.de) Overall design: 6 samples in 2 groups: N2, L4440 5 days (3 Samples); N2, T25B9.1 5 days (3 Samples)
Impairing L-Threonine Catabolism Promotes Healthspan through Methylglyoxal-Mediated Proteohormesis.
Sex, Age, Specimen part, Cell line, Subject
View SamplesThere is a growing body of evidence about the presence and the activity of the miRISC in the nucleus of mammalian cells. Here, we show by quantitative proteomic analysis that Ago2 interacts with nucleoplasmic Sfpq in a RNA-dependent fashion. By HITS-CLIP and transcriptomic analyses, we demonstrated that Sfpq directly controls the miRNA targeting of a subset of crucial miRNA-target mRNAs when it binds locally. Sfpq modulates miRNA targeting in both nucleoplasm and cytoplasm, indicating a nucleoplasmic imprinting of Sfpq-target mRNAs that influence miRNA targeting in both cellular compartments. Mechanistically, Sfpq binds to a sizeable set of long 3'UTR forming long aggregates to optimize miRNA position/recruitment to selected binding sites, as we show for Lin28A mRNA. These results extend the miRNA-mediated post-transcriptional gene silencing into the nucleoplasm and indicate that an unique Sfpq-dependent post-transcriptional strategy for controlling both nuclear and cytoplasmic gene expression takes place in cells during physio-pathological events. Overall design: RNA-seq of P19 cells control and upon SFPQ knockdown both in triplicates
Post-transcriptional gene silencing mediated by microRNAs is controlled by nucleoplasmic Sfpq.
Specimen part, Subject
View SamplesBackground: Arsenite is one of the most toxic chemical substances known and is assumed to exert detrimental effects on viability even at lowest concentrations. By contrast and unlike higher concentrations, we here find that exposure to low-dose arsenite promotes growth of cultured mammalian cells. In the nematode C. elegans, low-dose arsenite promotes resistance against thermal and chemical stressors, and extends lifespan of this metazoan, whereas higher concentrations reduce longevity. While arsenite causes a transient increase in reactive oxygen species (ROS) levels in C. elegans, co-exposure to ROS scavengers prevents the lifespan-extending capabilities of arsenite, indicating that transiently increased ROS levels act as transducers of arsenite effects on lifespan, a process known as mitohormesis. The RNA-seq data comprises 2 biological replicates for worms exposed to 100nM Arsenite 48h after L4 and 2 biological replicates of the same age as controls Jena Centre for Systems Biology of Ageing - JenAge (www.jenage.de) Overall design: 4 samples: 2 mRNA profiles of C.elegans 48h after L4 exposed to Arsenite; 2 mRNA profiles of C.elegans 48h after L4 as controls (H20). The N2 wild type (var. Bristol) strain was used.
Mitochondrial hormesis links low-dose arsenite exposure to lifespan extension.
Specimen part, Treatment, Subject
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Control of vertebrate multiciliogenesis by miR-449 through direct repression of the Delta/Notch pathway.
Specimen part
View SamplesWe used microarrays to detail the global programme of gene expression that occurs in response to miR-449 or miR-34 overexpression in proliferating HAECs.
Control of vertebrate multiciliogenesis by miR-449 through direct repression of the Delta/Notch pathway.
Specimen part
View Samples