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SRP075377
Homo sapiens
1600 Downloadable Samples
Illumina HiSeq 2500
Description
Pancreatic islet cells are critical for maintaining normal blood glucose levels and their malfunction underlies diabetes development and progression. We used single-cell RNA sequencing to determine the transcriptomes of 1,492 human pancreatic a-, ß-, d- and PP cells from non-diabetic and type 2 diabetes organ donors. We identified cell type specific genes and pathways as well as 245 genes with disturbed expression in type 2 diabetes. Importantly, 92% of the genes have not previously been associated with islet cell function or growth. Comparison of gene profiles in mouse and human a- and ß-cells revealed species-specific expression. All data are available for online browsing and download and will hopefully serve as a resource for the islet research community. Overall design: Single-cell RNA sequencing of human non-diabetic and type 2 diabetic pancreatic islet cells
Publication Title
RNA Sequencing of Single Human Islet Cells Reveals Type 2 Diabetes Genes.
Sample Metadata Fields
Sex, Age, Specimen part, Race, Subject
View Samples- Mus musculus
- 207 Downloadable Samples
- Illumina HiSeq 2500
Description
Aging improves pancreatic ß-cell function in mice. This is a surprising finding since aging is typically associated with functional decline. We performed single-cell RNA sequencing of ß-cells from 3 and 26 month old mice to explore how changes in gene expression contribute to improved function with age. The old mice were healthy, had reduced blood glucose levels and increased ß-cell mass, which correlated to their body weight. ß-cells from young and old mice had similar transcriptome profiles. In fact, only 193 genes (0.89% of all detected genes) were significantly regulated (= 2-fold; false discovery rate < 0.01; normalized counts > 5). Of these, 183 were downregulated and mainly associated with pathways regulating gene expression, cell cycle, cell death and survival as well as cellular movement, function and maintenance. Collectively, our data show that ß-cells from very old mice have transcriptome profiles similar to those of young mice. These data support previous findings that aging is not associated with reduced ß-cell mass or functional ß-cell decline in mice. Overall design: Single-cell RNA sequencing of mouse pancreatic islet beta cells
Publication Title
Single-Cell RNAseq Reveals That Pancreatic β-Cells From Very Old Male Mice Have a Young Gene Signature.
Sample Metadata Fields
Sex, Age, Specimen part, Subject
View Samples- Mus musculus
- 622 Downloadable Samples
- Illumina HiSeq 2500
Description
This study provides an assessment of the Fluidigm C1 platform for RNA sequencing of single mouse pancreatic islet cells. The system combines microfluidic technology and nanoliter-scale reactions. We sequenced 622 cells allowing identification of 341 islet cells with high-quality gene expression profiles. The cells clustered into populations of alpha-cells (5%), beta-cells (92%), delta-cells (1%) and PP-cells (2%). We identified cell-type specific transcription factors and pathways primarily involved in nutrient sensing and oxidation and cell signaling. Unexpectedly, 281 cells had to be removed from the analysis due to low viability (23%), low sequencing quality (13%) or contamination resulting in the detection of more than one islet hormone (64%). Collectively, we provide a resource for identification of high-quality gene expression datasets to help expand insights into genes and pathways characterizing islet cell types. We reveal limitations in the C1 Fluidigm cell capture process resulting in contaminated cells with altered gene expression patterns. This calls for caution when interpreting single-cell transcriptomics data using the C1 Fluidigm system. Overall design: Single-cell RNA sequencing of mouse C57BL/6 pancreatic islet cells
Publication Title
Use of the Fluidigm C1 platform for RNA sequencing of single mouse pancreatic islet cells.
Sample Metadata Fields
Specimen part, Cell line, Subject
View Samples- Homo sapiens
- 39 Downloadable Samples
Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
Atopic dermatitis (AD) is the most common inflammatory skin disease, with high unmet need for new therapies that are safe for chronic use. Emerging data suggest that TH2-cytokines play important roles in a variety of allergic and atopic conditions, including asthma and AD. In early phase clinical trials, dupilumab (a fully human monoclonal antibody against IL-4R that potently blocks IL-4 and IL-13 signaling) rapidly and markedly improved clinical measures in adults with either asthma (with elevated eosinophil counts) or moderate-to-severe AD. The pathomechanisms that may be impacted by IL-4/13 blockade in these disease settings have not yet been characterized in detail.
Publication Title
Dupilumab improves the molecular signature in skin of patients with moderate-to-severe atopic dermatitis.
Sample Metadata Fields
Specimen part, Treatment, Subject, Time
View Samples- Mus musculus
- 10 Downloadable Samples
- Illumina HiSeq 2500
Description
Glucagon supports glucose homeostasis by stimulating hepatic gluconeogenesis, in part by promoting the uptake and conversion of amino acids into gluconeogenic precursors. Genetic disruption or pharmacologic inhibition of glucagon signaling results in elevated plasma amino acids, and compensatory glucagon hypersecretion involving expansion of pancreatic a-cell mass. Regulation of pancreatic a- and ß-cell growth has drawn a lot of attention because of potential therapeutic implications. Recent findings indicate that hyperaminoacidemia triggers pancreatic a-cell proliferation via an mTOR-dependent pathway. We confirm and extend these findings by demonstrating that glucagon pathway blockade selectively increases expression of the sodium-coupled neutral amino acid transporter Slc38a5 in a subset of highly proliferative a-cells, and that Slc38a5 is critical for the pancreatic response to glucagon pathway blockade; most notably, mice deficient in Slc38a5 exhibit markedly decreased a-cell hyperplasia to glucagon pathway blockade-induced hyperaminoacidemia. These results show that Slc38a5 is a key component of the feedback circuit between glucagon receptor signaling in the liver and amino acid-dependent regulation of pancreatic a-cell mass in mice. Overall design: Examination of the transcriptomes of pancreatic islets of mice treated with GCGR-antibody and an isotype control antibody.
Publication Title
Amino Acid Transporter Slc38a5 Controls Glucagon Receptor Inhibition-Induced Pancreatic α Cell Hyperplasia in Mice.
Sample Metadata Fields
Specimen part, Cell line, Subject
View Samples- Mus musculus
- 6 Downloadable Samples
- Illumina HiSeq 2000
Description
Glucagon supports glucose homeostasis by stimulating hepatic gluconeogenesis, in part by promoting the uptake and conversion of amino acids into gluconeogenic precursors. Genetic disruption or pharmacologic inhibition of glucagon signaling results in elevated plasma amino acids and compensatory glucagon hypersecretion involving expansion of pancreatic a cell mass. Recent findings indicate that hyperaminoacidemia triggers pancreatic a cell proliferation via an mTOR-dependent pathway. We confirm and extend these findings by demonstrating that glucagon pathway blockade selectively increases expression of the sodium-coupled neutral amino acid transporter Slc38a5 in a subset of highly proliferative a cells and that Slc38a5 controls the pancreatic response to glucagon pathway blockade; most notably, mice deficient in Slc38a5 exhibit markedly decreased a cell hyperplasia to glucagon pathway blockade-induced hyperaminoacidemia. These results show that Slc38a5 is a key component of the feedback circuit between glucagon receptor signaling in the liver and amino-acid-dependent regulation of pancreatic a cell mass in mice. Overall design: Examination of the transcriptomes of islet non-beta-cells of GcgR knock out mice.
Publication Title
Amino Acid Transporter Slc38a5 Controls Glucagon Receptor Inhibition-Induced Pancreatic α Cell Hyperplasia in Mice.
Sample Metadata Fields
Sex, Specimen part, Cell line, Subject
View Samples- Homo sapiens
- 20 Downloadable Samples
- IlluminaHiSeq2500, IlluminaHiSeq2000
Description
High resolution transcriptional profiling of H1-derived human neuronal precursor cells over a timecourse of differentiation in vitro. Overall design: Human NPC differentiation timecourse covers Days 0,1,2,4,5,11, and 18 after induction of neuronal differentiation as described in manuscript. Each time point was assayed in triplicate cultures with the exception of Day 5, in which one outlier culture has been removed.
Publication Title
Multiple knockout mouse models reveal lincRNAs are required for life and brain development.
Sample Metadata Fields
No sample metadata fields
View Samples- Homo sapiens
- 116 Downloadable Samples
- Illumina HiSeq 2000
Description
Find the casual relationship between gene expression network and cellular phenotype at single cell resolution. We collected donated human pre-implatation embryos, and the embryonic stem cells derived from them, isolate individual cells, prepared single cell cDNAs, and sequenced them by HiSeq2000. Then we analyzed the expression of known RefSeq genes. Overall design: We get transcriptome of 124 individual cells from human pre-implantation embryos and human embryonic stem cells by applying single cell RNA-seq technique we recently developed[1][2][3][4]. We did in-depth bioinformatic analysis to these data and found very dynamic expression of protein-coding genes. [1] Tang, F. et al. (2010a) Tracing the Derivation of Embryonic Stem Cells from the Inner Cell Mass by Single-Cell RNA-Seq Analysis. Cell Stem Cell 6, 468-478. [2] Tang, F. et al. (2010b) RNA-Seq analysis to capture the transcriptome landscape of a single cell. Nat Protocols 5, 516-535. [3] Tang, F. et al. (2009) mRNA-Seq whole-transcriptome analysis of a single cell. Nat Meth 6, 377-382. [4] Tang, F. et al. (2011) Development and applications of single-cell transcriptome analysis. Nat Meth 8, S6-S11.
Publication Title
Single-cell RNA-Seq profiling of human preimplantation embryos and embryonic stem cells.
Sample Metadata Fields
Specimen part, Subject
View Samples- Homo sapiens
- 9 Downloadable Samples
- Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
Cryptosporidium hominis and parvum primarily infect intestinal epithelial cells, which, in turn, play a key role in activating and communicating with the host immune system. To determinate which genes are regulated during early infection of non-transformed human epithelial cells, human ileal mucosa was removed (from surgical specimens), placed on collagen membranes, and cultured as explants. Explant cultures were infected with C. parvum, C. hominis, or control culture medium. After 24 hrs, RNA was extracted and analyzed using Affmetrix GeneChip microarrays. Among the more prominent genes with regulated expression was Osteoprotegerin (OPG), which was increased in all of the explants at 24 hrs and further up-regulated 1.58 fold by C. parvum and 2.54 fold by C. hominis infection compared with uninfected explants. Using real time PCR, we confirmed a 3.14 and 3.79 fold increase in OPG mRNA after infection with C. parvum and C. hominis respectively.
Publication Title
Cryptosporidium infection of human intestinal epithelial cells increases expression of osteoprotegerin: a novel mechanism for evasion of host defenses.
Sample Metadata Fields
No sample metadata fields
View Samples- Homo sapiens
- 3 Downloadable Samples
- Illumina Genome Analyzer II
Description
An in-depth analysis of miRNomes in 3 human myeloid leukemia cell lines was carried out to comprehensively identify miRNAs that distinguish acute and chronic myeloid leukemias and relate to myeloid cell differentiation. Overall design: Characterization the miRNomes in 3 myeloid leukemia cell lines.
Publication Title
Characterization of miRNomes in acute and chronic myeloid leukemia cell lines.
Sample Metadata Fields
Specimen part, Disease, Cell line, Subject
View Samples