We applied RNA-seq analysis to human islet cells, received from 3 independent donors, treated with either redifferentiation cocktail + ARX shRNA, or redifferentiation cocktail + control shRNA or left untreated. Overall design: Examination of the effect of ARX inhibition on redifferentiation of ß-cell-derived (BCD) cells
Redifferentiation of expanded human islet β cells by inhibition of ARX.
No sample metadata fields
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Plasmacytoid dendritic cells and C1q differentially regulate inflammatory gene induction by lupus immune complexes.
Specimen part, Treatment, Subject
View SamplesThe goal of this study was to determine what genes are up- and down-regulated in response to lupus immune complexes in purified CD14+ monocyte stimulations. Our results have shown that novel genes are induced by immune complexes but the response is less robust when using purified monocytes versus total PBMCs
Plasmacytoid dendritic cells and C1q differentially regulate inflammatory gene induction by lupus immune complexes.
Specimen part, Treatment, Subject
View SamplesWe applied in parallel RNA-Seq and Ribosome-profiling analyses to immortalized human primary BJ fibroblast cells under the following conditions: normal proliferation, quiescence (induced by serum depletion), senescence (induced by activation of the oncogenic RASG12V gene, and examined at early (5 days; pre-senescent state) and late (14 days; fully senescent state) time points), and neoplastic transformation (induced by RASG12V in the background of stable p53 and p16INK4A knockdowns and SV40 small-T expression. Overall design: RNA-seq, using Illumina HiSeq 2000, was applied to BJ cells under 5 conditions: proliferation, quiescence, pre-senescence, full-senescence, and transfomed. Ribosome profiling, using Illumina HiSeq 2000, was applied to BJ cells under 5 conditions: proliferation, quiescence, pre-senescence, full-senescence, and transfomed.
p53 induces transcriptional and translational programs to suppress cell proliferation and growth.
No sample metadata fields
View SamplesWe applied in parallel RNA-Seq and Ribosome-profiling analyses to immortalized human primary BJ fibroblast cells in which p53 was induced by Nutlin-3a Overall design: RNA-seq, using Illumina HiSeq 2000, was applied to BJ cells treated with Nutlin-3a, at 5 timepoints: 0, 2, 4, 6, 19 hrs Ribosome profiling was applied to BJ cells treated with Nutlin-3a, at 5 timepoints: 0, 2, 4, 6, 19 hrs
p53 induces transcriptional and translational programs to suppress cell proliferation and growth.
No sample metadata fields
View SamplesWe used RNA-seq and Ribo-seq analyses to examine the effect of CPT treatment of translation efficiency (TE) Overall design: We measured expression levels (RNA.seq) and ribosome densities (ribo-seq) using biological duplicates of control and CPT-treated (5 hrs) MCF7 cells
Transcription Impacts the Efficiency of mRNA Translation via Co-transcriptional N6-adenosine Methylation.
No sample metadata fields
View SamplesWe used RNA-seq and Ribo-seq analyses to examine translation efficiency (TE) in PC9 and H1933 cells Overall design: We measured expression levels (RNA.seq) and ribosome densities (ribo-seq) in PC9 and H1933 cell lines
Transcription Impacts the Efficiency of mRNA Translation via Co-transcriptional N6-adenosine Methylation.
No sample metadata fields
View SamplesWe used RNA-seq and Ribo-seq analyses to examine the effect of Nutlin3a (activator of p53) treatment of translation efficiency (TE) Overall design: We measured expression levels (RNA.seq) and ribosome densities (ribo-seq) in control and Nutlin3a-treated (20 hrs) MCF7 cells
Transcription Impacts the Efficiency of mRNA Translation via Co-transcriptional N6-adenosine Methylation.
No sample metadata fields
View SamplesSystemic lupus erythematosus (SLE) is an autoimmune disorder characterized by the production of antibodies to self-nucleic acids, immune complex deposition and tissue inflammation such as glomerulonephritis. Innate recognition of molecular complexes containing self-DNA and RNA and the ensuing production of type I interferons (IFN) contribute to SLE development. Plasmacytoid dendritic cells (pDCs) have been proposed as a relevant source of pathogenic IFN in SLE; however, their net contribution to the disease remains unclear. We addressed this question using haplodeficiency of the pDC-specific transcription factor E2-2 (Tcf4), which causes a specific impairment of pDC function in otherwise normal animals. We report that Tcf4+/- animals were significantly protected from SLE-like disease caused by the overexpression of the endosomal RNA sensor Tlr7. The protection was also observed after the monoallelic deletion of Tcf4 specifically in the dendritic cell lineage. Furthermore, Tcf4 haplodeficiency in the B6.Sle1.Sle3 multigenic model of SLE ameliorated key disease manifestations including anti-DNA antibody production, immune activation and glomerulonephritis. These results provide genetic evidence that pDCs are critically involved in SLE pathogenesis, confirming their potential utility as therapeutic targets in the disease.
Genetic evidence for the role of plasmacytoid dendritic cells in systemic lupus erythematosus.
Sex, Specimen part
View SamplesThe Gfi1-Cre mouse is commonly used for conditional hair cell-specific gene deletion/activation in the inner ear. However, we have shown that these mice produce a pattern of recombination that is not strictly limited to hair cells, and that Gfi1cre/+ mice exhibit an early onset progressive hearing loss as compared with their wildtype littermates. Here we performed a transcriptome analysis of Gfi1cre/+ and Gfi1+/+ cochlea to detect potential changes in gene expression that could contribute to their hearing loss phenotype, or that could potentially confound downstream analysis of conditional gene deletion using these mice. Overall design: Trancriptome profiles of P8 cochlear duct from mice of two genotype - Gfi1cre/+ and Gfi+/+ controls - were measured. Gene expression levels were recorded in independent triplicates using polyA-enriched RNA-seq
Gfi1<sup>Cre</sup> mice have early onset progressive hearing loss and induce recombination in numerous inner ear non-hair cells.
Specimen part, Cell line, Subject
View Samples