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accession-icon SRP064187
Redifferentiation of expanded human islet ß cells by inhibition of ARX
  • organism-icon Homo sapiens
  • sample-icon 9 Downloadable Samples
  • Technology Badge IconIlluminaHiSeq2500

Description

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

Publication Title

Redifferentiation of expanded human islet β cells by inhibition of ARX.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE32285
Genome-wide analysis of lupus immune complex stimulation and how this response is regulated by C1q
  • organism-icon Homo sapiens
  • sample-icon 8 Downloadable Samples
  • Technology Badge IconIllumina HumanRef-8 v3.0 expression beadchip

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Plasmacytoid dendritic cells and C1q differentially regulate inflammatory gene induction by lupus immune complexes.

Sample Metadata Fields

Specimen part, Treatment, Subject

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accession-icon GSE32278
Genome-wide analysis of lupus immune complex stimulation of purified CD14+ monocytes and how this response is regulated by C1q
  • organism-icon Homo sapiens
  • sample-icon 8 Downloadable Samples
  • Technology Badge IconIllumina HumanRef-8 v3.0 expression beadchip

Description

The 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

Publication Title

Plasmacytoid dendritic cells and C1q differentially regulate inflammatory gene induction by lupus immune complexes.

Sample Metadata Fields

Specimen part, Treatment, Subject

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accession-icon SRP017378
Transcriptome-profiling (RNA-seq) and Ribosome-profiling (Ribo-seq) in proliferation, quiescence, senescence and transformed states.
  • organism-icon Homo sapiens
  • sample-icon 9 Downloadable Samples
  • Technology Badge Icon

Description

We 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.

Publication Title

p53 induces transcriptional and translational programs to suppress cell proliferation and growth.

Sample Metadata Fields

No sample metadata fields

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accession-icon SRP020544
Transcriptome-profiling (RNA-seq) and Ribosome-profiling (Ribo-seq) of BJ cells treated with Nutlin-3a, an MDM2 inhibitor, which induces p53.
  • organism-icon Homo sapiens
  • sample-icon 5 Downloadable Samples
  • Technology Badge Icon

Description

We 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

Publication Title

p53 induces transcriptional and translational programs to suppress cell proliferation and growth.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon SRP101952
RNA_seq and Ribo_seq analyses of control and CPT-treated MCF7 cells
  • organism-icon Homo sapiens
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon

Description

We 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

Publication Title

Transcription Impacts the Efficiency of mRNA Translation via Co-transcriptional N6-adenosine Methylation.

Sample Metadata Fields

No sample metadata fields

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accession-icon SRP102021
RNA_seq and Ribo_seq analyses applied to PC9 and H1933 human cancer cell lines
  • organism-icon Homo sapiens
  • sample-icon 2 Downloadable Samples
  • Technology Badge Icon

Description

We 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

Publication Title

Transcription Impacts the Efficiency of mRNA Translation via Co-transcriptional N6-adenosine Methylation.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon SRP102020
RNA_seq and Ribo_seq analyses of control and Nutlin3a-treated MCF7 cells (20 hrs)
  • organism-icon Homo sapiens
  • sample-icon 2 Downloadable Samples
  • Technology Badge Icon

Description

We 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

Publication Title

Transcription Impacts the Efficiency of mRNA Translation via Co-transcriptional N6-adenosine Methylation.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE57324
Gene expression analysis in the spleen of wild type, Sle1.3 (lupus mice) and Sle1.3 mice haplodeficient for E2-2 (exhibiting non functional pDCs)
  • organism-icon Mus musculus
  • sample-icon 8 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

Systemic 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.

Publication Title

Genetic evidence for the role of plasmacytoid dendritic cells in systemic lupus erythematosus.

Sample Metadata Fields

Sex, Specimen part

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accession-icon SRP081314
Expression profiling of cochlear ducts from P8 Gfi1cre/+ and Gfi1+/+ mice
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

The 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

Publication Title

Gfi1<sup>Cre</sup> mice have early onset progressive hearing loss and induce recombination in numerous inner ear non-hair cells.

Sample Metadata Fields

Specimen part, Cell line, Subject

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refine.bio is a repository of uniformly processed and normalized, ready-to-use transcriptome data from publicly available sources. refine.bio is a project of the Childhood Cancer Data Lab (CCDL)

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Cite refine.bio

Casey S. Greene, Dongbo Hu, Richard W. W. Jones, Stephanie Liu, David S. Mejia, Rob Patro, Stephen R. Piccolo, Ariel Rodriguez Romero, Hirak Sarkar, Candace L. Savonen, Jaclyn N. Taroni, William E. Vauclain, Deepashree Venkatesh Prasad, Kurt G. Wheeler. refine.bio: a resource of uniformly processed publicly available gene expression datasets.
URL: https://www.refine.bio

Note that the contributor list is in alphabetical order as we prepare a manuscript for submission.

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