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GSE77424
Mus musculus
12 Downloadable Samples
Illumina mouseref-8_v2_0_r3 expression beadchip
Description
This SuperSeries is composed of the SubSeries listed below.
Publication Title
PDGF Engages an E2F-USP1 Signaling Pathway to Support ID2-Mediated Survival of Proneural Glioma Cells.
Sample Metadata Fields
Specimen part, Treatment
View Samples- Mus musculus
- 6 Downloadable Samples
Illumina mouseref-8_v2_0_r3 expression beadchip
Description
Identification of critical survival determinants of PDGF-driven proneural glioma. Results provided information about the genes and pathways that are regulated by PDGF signaling in PDGF-driven proneural glioma and led to the assessment of the importance of the USP1-ID2 axis in proneural glioma.
Publication Title
PDGF Engages an E2F-USP1 Signaling Pathway to Support ID2-Mediated Survival of Proneural Glioma Cells.
Sample Metadata Fields
Specimen part, Treatment
View Samples- Mus musculus
- 6 Downloadable Samples
- Illumina mouseref-8_v2_0_r3 expression beadchip
Description
Identification of critical survival determinants of PDGF-driven proneural glioma. Results provided information about the genes and pathways that are regulated by PDGF signaling in PDGF-driven proneural glioma and led to the assessment of the importance of the USP1-ID2 axis in proneural glioma.
Publication Title
PDGF Engages an E2F-USP1 Signaling Pathway to Support ID2-Mediated Survival of Proneural Glioma Cells.
Sample Metadata Fields
Specimen part
View Samples- Mus musculus
- 8 Downloadable Samples
- Affymetrix Murine Genome U74A Version 2 Array (mgu74av2)
Description
Mouse strains have been identified that are resistant (i.e. DBA/2) or susceptible (i.e. C57BL/6) to infection from pathogenic fungus Coccidioides immitis. However, the genetic and immunological basis for this difference has not been fully characterized.
Publication Title
Factors regulated by interferon gamma and hypoxia-inducible factor 1A contribute to responses that protect mice from Coccidioides immitis infection.
Sample Metadata Fields
Specimen part
View Samples- Homo sapiens
- 2 Downloadable Samples
IlluminaHiSeq2000
Description
Analysis of p53 binding sites using multiplex enhancer reporter assays, ChIP-seq data and RNA-seq data. Transcription factors establish and maintain the specific transcriptome of a cell by binding to genomic regulatory regions, thereby regulating the transcription of their target genes. Like many transcription factors, the DNA sequence-specific binding preferences of p53 are known. However, it remains largely unclear what distinguishes functional enhancers from other bound genomic regions that have no regulatory activity. In addition, the genome is scattered with seemingly perfect recognition sequences that remain unoccupied. To disentangle the rules of genome-wide p53 binding, we employed two complementary techniques of multiplex enhancer-reporter assays, one using barcoded reporters and the other using enhancer self-transcription. We compared the activity of more than one thousand candidate p53 enhancers under loss and gain of p53 conditions and identified several hundred high-confidence p53-responsive enhancers. Strikingly, the large majority (99%) of these target enhancers can be characterized and distinguished from negative sequences by the occurrence of a single p53 binding site. By training a machine learning classifier on these data, and integrating the resulting genome-wide predictions with fifteen publicly available human p53 ChIP-seq data sets, we identified a consensus set of 1148 functional p53 binding sites in the human genome. Unexpectedly, this direct p53 cistrome is invariably used between cell types and experimental conditions, while differences between experiments can be largely attributed to indirect non-functional binding. Our data suggest that direct p53 enhancers function in a context-independent manner and do not contain obvious combinatorial complexity of binding sites for multiple transcription factors. They represent a class of unsophisticated cell-autonomous enhancers with a single binding site, distinct from complex developmental enhancers that integrate signals from multiple transcription factors. This suggests that context-dependent regulation of p53 target genes is not encoded in the p53 enhancer, but at different upstream or downstream layers of the cell''s gene regulatory network. Overall design: RNA-seq on MCF7 cells with p53 stable knockdown.
Publication Title
Multiplex enhancer-reporter assays uncover unsophisticated TP53 enhancer logic.
Sample Metadata Fields
No sample metadata fields
View Samples- Mus musculus
- 6 Downloadable Samples
- Affymetrix Mouse Genome 430 2.0 Array (mouse4302)
Description
Bone marrow-derived dendritic cells from C57BL/6 mice were treated with 1 ug/ml cholera toxin, 10 uM forskolin or control medium for 2 h.
Publication Title
Mucosal adjuvant activity of cholera toxin requires Th17 cells and protects against inhalation anthrax.
Sample Metadata Fields
No sample metadata fields
View Samples- Homo sapiens
- 4 Downloadable Samples
- Illumina HiSeq 2000
Description
RNA-seq and ChIP-seq on MCF-7 breast cancer cell line upon activation of p53 by the non-genotoxic small molecule Nutlin-3a Overall design: RNA-seq on MCF7 without (NS) or with Nutlin-3a stimulation (S), in duplicate, using illumina HiSeq 2000
Publication Title
iRegulon: from a gene list to a gene regulatory network using large motif and track collections.
Sample Metadata Fields
Specimen part, Cell line, Subject
View Samples- Mus musculus
- 6 Downloadable Samples
- Illumina HiSeq 2500
Description
Somatic ribosomal protein defects have recently been described in cancer, yet their impact on cellular transcription and translation remain poorly understood. Here we integrated mRNA sequencing, ribosome footprinting, polysomal RNA seq and quantitative mass spectrometry datasets obtained from an isogenic mouse lymphoid cell model in order to study the T-cell acute lymphoblastic leukemia (T-ALL) associated R98S mutation in ribosomal protein L10 (RPL10 R98S). RPL10 R98S induced changes in protein levels were to a much larger extent caused by transcriptional then translational changes and RPL10 R98S cells showed a gene signature corresponding to deregulation of hematopoietic transcription factors. Phosphoserine phosphatase (PSPH), a key enzyme in serine biosynthesis, displayed elevated transcription and translation and was one of the proteins showing the strongest upregulation in RPL10 R98S cells. Increased Psph protein levels were confirmed in RPL10 R98S engineered JURKAT cells and in hematopoietic cell cultures derived from Rpl10 R98S knock-in mice. Moreover, elevated serine and glycine biosynthesis in RPL10 R98S cells was supported by metabolic flux analyses. Analysis of PSPH expression levels in T-ALL patient samples revealed that PSPH upregulation is a generalized phenomenon in this disease, associated with elevated circulating serine and glycine levels. Addition of serine and glycine enhanced survival of stromal and myeloid cells, suggesting supportive effects on the hematopoietic niche. Finally, reduction of PSPH expression levels in T-ALL cell lines suppressed their in vitro proliferation and their capacity to expand in T-ALL xenograft models. In conclusion, transcriptome, translatome and proteome analysis of the RPL10 R98S mutation identified RPL10 R98S driven induction of cellular serine biosynthesis. Whereas serine metabolism has been implicated in cancer via PHGDH amplification, this is the first report supporting dependence of ALL cells on the serine biosynthesis enzyme PSPH. Overall design: 3 biological replicates for each condition (RPL10 R98S, RPL10 WT)
Publication Title
Translatome analysis reveals altered serine and glycine metabolism in T-cell acute lymphoblastic leukemia cells.
Sample Metadata Fields
Specimen part, Subject
View Samples- Caenorhabditis elegans
- 53 Downloadable Samples
- Illumina HiSeq 2000
Description
The Caenorhabditis elegans oxidative stress response transcription factor, SKN-1, is essential for the maintenance of redox homeostasis and is a functional ortholog of the Nrf family of transcription factors. The numerous levels of regulation that govern these transcription factors underscore their importance. Here, we add a thioredoxin, encoded by trx-1, to the expansive list of SKN-1 regulators. We report that loss of trx-1 promotes nuclear localization of intestinal SKN-1 in a redox-independent, cell non-autonomous fashion from the ASJ neurons. Furthermore, this regulation is not general to the thioredoxin family, as two other C. elegans thioredoxins TRX-2 and TRX-3 do not play a role in this process. Moreover, TRX-1-dependent regulation requires signaling from the p38 MAPK signaling pathway. However, while TRX-1 regulates SKN-1 nuclear localization, SKN-1 transcriptional activity remains largely unaffected. Interestingly, RNA-Seq revealed that loss of trx-1 elicits a general, organism-wide down-regulation of several classes of genes; those encoding for collagens and lipid transport and localization being most prevalent. However, one prominent lipase-related gene, lips-6, is highly up regulated upon loss of trx-1 in a skn-1-dependent manner. Together, these results uncover a novel role for a thioredoxin in regulating intestinal SKN-1 nuclear localization in a cell non-autonomous manner, thereby contributing to the understanding of the processes involved in maintaining redox homeostasis throughout an organism. Overall design: Four samples were analyzed: Two nematode strains were analyzed, each under non-stressed and stressed (10mM NaAs) conditions
Publication Title
TRX-1 Regulates SKN-1 Nuclear Localization Cell Non-autonomously in Caenorhabditis elegans.
Sample Metadata Fields
Disease, Cell line, Subject
View Samples- Homo sapiens
- 8 Downloadable Samples
- Illumina HiSeq 2000
Description
RNAseq analysis of human bone marrow derived stromal cells (MSCs) treated for 24 hours with or wihout 10ng/ml Fibroblast Growth Factor 2 (FGF2) MSCs were derived from 4 different healthy donors. Cells were expanded to passage 3-4. Then cells were treated with FGF-2. 24 hours later, total RNA was extracted (total 8 samples). Overall design: RNA was submitted to BGI Americas for RNAseq. Here, QC was performed using Agilent 2100. All samples had a RIN above 8.0. For preparation for library, mRNA was enriched by using the oligo (dT) magnetic beads. mRNA was enriched by using the oligo (dT) magnetic beads. mRNA was fragmented into short fragments (about 200bp) using a fragmentation buffer. Then the first strand of cDNA was synthesized by random hexamer-primer using the mRNA fragments as templates. Buffer, dNTSPs, RNase H and DNA polymerase I were added to synthesize the second strand. The double strand cDNA was purified with QiaQuick PCR extraction kit and washed with EB buffer for end repair and base A addition. Finally, sequencing adapters were ligated to the fragments. The fragments are purified by Agarose gel electrophoresis and enriched by PCR amplification. The library products are ready for sequencing analysis via 2 sE50 lanes in Illumina HiSeqâ„¢ 2000.
Publication Title
FGF2 Induces Migration of Human Bone Marrow Stromal Cells by Increasing Core Fucosylations on N-Glycans of Integrins.
Sample Metadata Fields
Specimen part, Treatment, Subject
View Samples