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Homo sapiens
15 Downloadable Samples
NextSeq 500
Description
To understand the biological mechanism of ELL2 in multiple myeloma (MM), we show that the MM risk allele lowers ELL2 expression in CD138+ plasma cells (Pcombined=2.5×10-27; bcombined=-0.24 s.d.), but not in peripheral blood or other tissues. Consistent with this, several variants representing the MM risk allele map to regulatory genomic regions, and three yield reduced transcriptional activity in plasmocytoma cell lines. One of these (rs3777189-C) co-locates with the best-supported lead variants for ELL2 expression and MM risk, and reduces binding of MAFF/G/K family transcription factors. Moreover, further analysis reveals that the MM risk allele associates with upregulation of gene sets related to ribosome biogenesis, and knockout/knockdown and rescue experiments in plasmocytoma cell lines support a cause-effect relationship. Overall design: Reconstitution of ELL2 expression in L363-ELL2-knockout cells
Publication Title
The multiple myeloma risk allele at 5q15 lowers ELL2 expression and increases ribosomal gene expression.
Sample Metadata Fields
Specimen part, Disease, Disease stage, Cell line, Treatment, Subject
View Samples- Homo sapiens
- 6 Downloadable Samples
- NextSeq 500
Description
To understand the biological mechanism of ELL2 in multiple myeloma (MM), we show that the MM risk allele lowers ELL2 expression in CD138+ plasma cells (Pcombined=2.5×10-27; bcombined=-0.24 s.d.), but not in peripheral blood or other tissues. Consistent with this, several variants representing the MM risk allele map to regulatory genomic regions, and three yield reduced transcriptional activity in plasmocytoma cell lines. One of these (rs3777189-C) co-locates with the best-supported lead variants for ELL2 expression and MM risk, and reduces binding of MAFF/G/K family transcription factors. Moreover, further analysis reveals that the MM risk allele associates with upregulation of gene sets related to ribosome biogenesis, and knockout/knockdown and rescue experiments in plasmocytoma cell lines support a cause-effect relationship. Overall design: knock out ELL2 in L363 cells using CRISPR-Cas9
Publication Title
The multiple myeloma risk allele at 5q15 lowers ELL2 expression and increases ribosomal gene expression.
Sample Metadata Fields
Disease, Disease stage, Cell line, Subject
View Samples
GSE55902- Oryza sativa
- 6 Downloadable Samples
Affymetrix Rice Genome Array (rice)
Description
Senescence is a developmental process and chlorophyll is an indicator of leaf senescene. In plants cytokinin plays a role in delaying leaf senescence. Chlorophyll degradation is tightly regulated during senescence and cytokinin might interplay in the chrorophyll degradation pathway to regulate leaf greening.
Publication Title
Cytokinin delays dark-induced senescence in rice by maintaining the chlorophyll cycle and photosynthetic complexes.
Sample Metadata Fields
Specimen part
View Samples- Rattus norvegicus
- 12 Downloadable Samples
- Affymetrix Rat Gene 2.0 ST Array (ragene20st)
Description
Intravesical BCG Immunotherapy is the standard of care in treating non-muscle invasive bladder cancer, yet its mechanism of action remains elusive. Both innate and adaptive immune responses have been implicated in BCG activity. While prior research has indirectly demonstrated the importance of T cells and shown a rise in CD4+ T cells in bladder tissue after BCG, T cell subpopulations have not been fully characterized. We investigated the relationship between effector and regulatory T cells in an immune competent, clinically relevant rodent model of bladder cancer. Our data demonstrate that cancer progression in the MNU rat model of bladder cancer is characterized by a decline in the CD8/FoxP3 ratio, consistent with decreased adaptive immunity. By contrast, treatment with intravesical BCG leads to a large, transient rise in the CD4+ T cell population in the urothelium, and is both more effective and immunogenic compared to intravesical chemotherapy. Interestingly, whole transcriptome expression profiling of post-treatment intravesical CD4+ and CD8+ T cells revealed minimal differences in gene expression after BCG treatment. Together, our results suggest that while BCG induces T cell recruitment to the bladder, the T cell phenotype does not markedly change, implying that combining T cell activating agents with BCG might improve clinical activity.
Publication Title
Intravesical BCG Induces CD4<sup>+</sup> T-Cell Expansion in an Immune Competent Model of Bladder Cancer.
Sample Metadata Fields
Specimen part, Treatment
View Samples- Drosophila melanogaster
- 3 Downloadable Samples
- Affymetrix Drosophila Genome Array (drosgenome1)
Description
Mutant embryos lacking maternal and zygotic HOW exhibit defects in mesoderm development. How is an RNA binding protein that regulates the levels of mRNAs by controling RNA metabolism.
Publication Title
Post-transcriptional repression of the Drosophila midkine and pleiotrophin homolog miple by HOW is essential for correct mesoderm spreading.
Sample Metadata Fields
No sample metadata fields
View Samples- Homo sapiens
- 39 Downloadable Samples
- Illumina HiSeq 2500
Description
In this accession we provide pseudouridylation measurements upon knockdown and/or overexpression three pseudouridine synthases, two of which (TRUB1 and PUS7) we find to be with predominant activity on mammalian mRNA. Overall design: Examination of pseudouridylation upon genetic perturbation of three pseudouridine synthases
Publication Title
TRUB1 is the predominant pseudouridine synthase acting on mammalian mRNA via a predictable and conserved code.
Sample Metadata Fields
Cell line, Treatment, Subject
View Samples- Homo sapiens
- 12 Downloadable Samples
- Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
Homeostatic programs maintain equilibrium between immune protection, and selftolerance. Such mechanisms impact autoimmunity and tumor formation, respectively. How tissue homeostasis is maintained, and impacts tumor surveillance is unknown. Here we identify that mononuclear phagocytes share conserved programming during homeostatic differentiation, and entry into tissue. IFN is necessary and sufficient to induce these transcripts, revealing a key instructive role. Remarkably, homeostatic and IFN-dependent programs enrich across primary human tumors, including melanoma, and stratify metastatic melanoma survival. Single-cell RNA-sequencing reveals enrichment of these modules in monocytes and DCs in human metastatic melanoma. Suppressor-of-cytokine-2 (SOCS2), a highly conserved transcript in this program is induced by IFN, and expressed in mononuclear phagocytes infiltrating primary melanoma. SOCS2 limits DC adaptive anti-tumoral immunity and T cell priming in vivo, indicating a critical regulatory role. Our findings link homeostasis in peripheral tissue to anti-tumoral immunity and escape, revealing coopting of tissue-specific immune development in the tumor microenvironment.
Publication Title
IFNγ-Dependent Tissue-Immune Homeostasis Is Co-opted in the Tumor Microenvironment.
Sample Metadata Fields
Specimen part, Disease, Disease stage
View Samples- Homo sapiens
- 519 Downloadable Samples
- Affymetrix HT HG-U133+ PM Array Plate (hthgu133pluspm)
Description
Whole blood expression was profiled in Rheumatoid Arthiritis and SLE (Systemic LUPUS Erythomatosus) patients.
Publication Title
Lymphotoxin-LIGHT pathway regulates the interferon signature in rheumatoid arthritis.
Sample Metadata Fields
Specimen part, Disease, Time
View Samples- Rattus norvegicus
- 9 Downloadable Samples
- Affymetrix Rat Gene 2.1 ST Array (ragene21st)
Description
Signalling via the colony stimulating factor 1 receptor (CSF1R) controls the survival, differentiation and proliferation of macrophages which are a source of the somatic growth factor insulin growth factor 1 (IGF1). Treatment of newborn mice with CSF1 has previously been shown to produce an increase in somatic growth rate and we hypothesised that treatment of neonatal low birth weight (LBW) rats with CSF1 would do the same. Growth rates were not affected, yet CSF1 treatment caused an unexpectedly large, but reversible increase in liver size and hepatic fat deposition in both normal and LBW rats. By transcriptional profiling, we have highlighted numerous CSF1-regulated genes known to be involved in lipid droplet formation in the liver and novel candidate genes for further investigation. In contrast to mice and weaner pigs, CSF1 treatment did not increase hepatocyte proliferation in neonatal rats, rather the data were consistent with increased macrophage proliferation instead. This suggests that Kupffer cells promote lipid accumulation in neonates and treatment to ablate CSF1R signalling may reverse lipid accumulation in the liver.
Publication Title
Macrophage colony-stimulating factor increases hepatic macrophage content, liver growth, and lipid accumulation in neonatal rats.
Sample Metadata Fields
Specimen part, Treatment
View Samples- Mus musculus
- 10 Downloadable Samples
- NextSeq 500
Description
N6-methyladenosine (m6A) is the most abundant modification on mRNA, and is implicated in critical roles in development, physiology and disease. A major challenge in the field has been the inability to quantify m6A stoichiometry and the lack of antibody-independent methodologies for interrogating m6A. Here, we develop MASTER-seq for systematic quantitative profiling of m6A at single nucleotide resolution, building on differential cleavage by an RNAse at methylated sites. MASTER-seq permitted validation and de novo discovery of m6A sites, calibration of the performance of antibody based approaches, and quantitative tracking of m6A dynamics in yeast gametogenesis and mammalian differentiation. We discover that m6A stoichiometry is 'hard-coded' in cis via a simple and predictable code. This code accounts for ~50% of the variability in methylation levels and allows accurate prediction of m6A loss/acquisition events across evolution. MASTER-seq will allow quantitative investigation of m6A regulation in diverse cell types and disease states. Overall design: 10 samples were analyzed: EBS WT and Metll3 -/- with two replicates each and ESC WT and Mettld -/- with three replicates
Publication Title
Deciphering the "m<sup>6</sup>A Code" via Antibody-Independent Quantitative Profiling.
Sample Metadata Fields
Specimen part, Subject
View Samples