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Homo sapiens
4 Downloadable Samples
NextSeq 500
Description
We performed morphogen-directed differentiation of human PSCs into HE followed by combinatorial screening of 26 candidate HSC-specifying TFs for the potential to promote hematopoietic engraftment in irradiated immune deficient murine hosts. We recovered seven TFs (ERG, HOXA5, HOXA9, HOXA10, LCOR, RUNX1, SPI1) that together were sufficient to convert HE into hematopoietic stem and progenitor cells (HSPCs) that engraft primary and secondary murine recipients Overall design: Examination of expression pattern in hematopoietic cells.
Publication Title
Haematopoietic stem and progenitor cells from human pluripotent stem cells.
Sample Metadata Fields
Specimen part, Subject
View Samples- Mus musculus
- 23 Downloadable Samples
Affymetrix Murine Genome U74A Version 2 Array (mgu74av2)
Description
We carried out a global survey of age-related changes in mRNA levels in the C57BL/6NIA mouse hippocampus and found a difference in the hippocampal gene expression profile between 2-month-old young mice and 15-month-old middle-aged mice correlated with an age-related cognitive deficit in hippocampal-based explicit memory formation. Middle-aged mice displayed a mild but specific deficit in spatial memory in the Morris water maze.
Publication Title
Altered hippocampal transcript profile accompanies an age-related spatial memory deficit in mice.
Sample Metadata Fields
Sex, Age, Specimen part
View Samples
SRP158145- Mus musculus
- 4 Downloadable Samples
- Illumina HiSeq 2000
Description
RNA transcriptome difference between WT and SFR KO iNKT cells To understand how SLAM family receptors (SFRs) contribute to iNKT cell development, a mouse lacking all SFRs in addition to the ligand of 2B4, CD48, was generated, and the transcriptional profiles of thymic iNKT cells from wild-type and SFR KO mice were compared, using RNA sequencing. Overall design: Examine RNA expression in WT and SFR KO iNKT cells Thymocytes were isolated from WT and SFR KO mice, and iNKT cells were enriched by negative selection. Unwanted cells (CD11b+ CD11c+ Gr-1+ Ter-119+ CD19+ CD8a+ cells) were targeted for removal with biotinylated antibodies (BioLegend), streptavidin-coated magnetic particles (RapidSpheres) and EasySep magnet (STEMCELL), and followed by staining with mCD1d/PBS-57 and anti-TCR. Then, iNKT cells were sorted with BD FACSAria III (BD Biosciences), and total RNA was isolated from sorted cells according to the manufacturer's instructions using the RNeasy plus micro kit (Qiagen). RNA-Seq library preparation was performed using the Illumina TruSeq Stranded mRNA Kit, according to manufacturer's instructions, and sequenced with Illumina HiSeq 2000 Sequencer. Read quality was confirmed using FastQC v0.10.1 before alignment using TopHat v2.0.10 on the mouse GRCm38/mm10 genome.
Publication Title
SLAM receptors foster iNKT cell development by reducing TCR signal strength after positive selection.
Sample Metadata Fields
Specimen part, Subject
View Samples- Mus musculus
- 9 Downloadable Samples
- Affymetrix Mouse Gene 1.0 ST Array (mogene10st)
Description
A suggested role for fibrillr collagen topology in the pregnancy-induced protection and invasive phenotype.
Publication Title
Collagen architecture in pregnancy-induced protection from breast cancer.
Sample Metadata Fields
Cell line
View Samples- Homo sapiens
- 2 Downloadable Samples
- IlluminaHiSeq2500
Description
Alterations in chromatin modifications, including DNA methylation and histone modification patterns, have been characterized under exposure of several environmental pollutants, including nickel. As with other carcinogenic metals, the mutagenic potential of nickel compounds is low and is not well correlated with its carcinogenic effects. Nickel exposure, however, is associated with alterations in chromatin modifications and related transcriptional programs, suggesting an alternative pathway whereby nickel exposure can lead to disease. To investigate the extent to which nickel exposure disrupts chromatin patterns, we profiled several histone modifications, including H3K4me3, H3K9ac, H3K27me3 and H3K9me2 as well as the insulator binding protein CTCF and the transcriptomes of control BEAS-2B cells and cells treated with nickel for 72 hours. Our results show significant alterations of the repressive histone modification H3K9me2 in nickel-exposed cells with spreading of H3K9me2 into new domains associated with gene silencing. We furthermore show that local regions of active chromatin can protect genes from nickel-induced H3K9me2 spreading. Interestingly, we show that nickel exposure selectively disrupts weaker CTCF sites, leading to spreading of H3K9me2 at these regions. These results have major implications in the understanding of how environmental carcinogens can affect chromatin dynamics and the consequences of chromatin domain disruption in disease progression. Overall design: Treat BEAS-2B cells with NiCl2 for 72 hours and compare histone modification, CTCF binding to control BEAS-2B cells to see how they regulated gene expression by RNA-seq
Publication Title
Epigenetic dysregulation by nickel through repressive chromatin domain disruption.
Sample Metadata Fields
No sample metadata fields
View Samples- Mus musculus
- 2 Downloadable Samples
- Illumina HiSeq 2500
Description
Purpose: The goal of this study was to identify the gene expression profile of mouse retina which carries deletions in Dnmt1, Dnmt3a and Dnmt3b genes. Method: Retinal mRNA profiles of Postnatal day 15 wild type mice and Dnmt1, Dnmt3a and Dnmt3b mutant mice were generated by deep-sequencing Overall design: Retinal mRNA profiles of post natal day 15 wild type and mutant mice with Illumina HiSeq 2500
Publication Title
Dnmt1, Dnmt3a and Dnmt3b cooperate in photoreceptor and outer plexiform layer development in the mammalian retina.
Sample Metadata Fields
Specimen part, Cell line, Subject
View Samples- Mus musculus
- 36 Downloadable Samples
- Affymetrix Mouse Gene 1.0 ST Array (mogene10st)
Description
Multipotent progenitors (MPP) and common dendritic cell progenitors (CDP) were obtained from mouse bone marrow, followed by in vitro culture with a specific cytokine cocktail and FACS sorting (Felker et al., 2010; Ser et al., 2012). Cells were treated with 10 ng/ml recombinant human TGF-1 (R&D Systems, Minneapolis, USA) for 2, 4, 8, 12 and 24 h as described (Felker et al., 2010) or left untreated.
Publication Title
TGF-β stimulation in human and murine cells reveals commonly affected biological processes and pathways at transcription level.
Sample Metadata Fields
Specimen part
View Samples- Mus musculus
- 18 Downloadable Samples
- Affymetrix Mouse Gene 2.0 ST Array (mogene20st)
Description
The NF-B pathway is a master regulator of inflammatory processes and is implicated in insulin resistance and pancreatic beta cell dysfunction in the metabolic syndrome. While canonical NF-B signaling is well studied, there is little information on the divergent non-canonical NF-B pathway in the context of pancreatic islet dysfunction in diabetes. Here, we demonstrate that pharmacological activation of the non-canonical NF-B inducing kinase (NIK) disrupts glucose homeostasis in zebrafish in vivo. Further, we identify NIK as a critical negative regulator of beta cell function as pharmacological NIK activation results in impaired glucose-stimulated insulin secretion in mouse and human islets. NIK levels are elevated in pancreatic islets isolated from diet-induced obese (DIO) mice, which exhibit increased processing of non-canonical NF-B components p100 to p52, and accumulation of RelB. Tumor necrosis factor (TNF) and receptor activator of NF-B ligand (RANKL), two ligands associated with diabetes, induce NIK in islets. Mice with constitutive beta cell intrinsic NIK activation present impaired insulin secretion with DIO. NIK activation triggers the non-canonical NF-B transcriptional network to induce genes identified in human type 2 diabetes genome-wide association studies linked to beta cell failure. These studies reveal that NIK contributes a central mechanism for beta cell failure in diet-induced obesity.
Publication Title
Nuclear factor κB-inducing kinase activation as a mechanism of pancreatic β cell failure in obesity.
Sample Metadata Fields
Specimen part, Treatment
View Samples- Homo sapiens
- 18 Downloadable Samples
- Affymetrix Human Gene 1.0 ST Array (hugene10st)
Description
We here compared gene expression profiles in HepG2 cells upon stimulation with 1 ng/ml TGF-beta1 for 20 min, 1 hour, 2 hours, 4 hours, and 24 hours with untreated control cells. Experiments were done in three independent replicates. The goal of this study was to determine genes regulated by TGF-beta1.HepG2 cells were obtained from DSMZ (Braunschweig, Germany) and cell identity confirmed by STR profiling using the AmpFlSTR Identfiler Direct PCR Amplification kit (Life Technologies, Darmstadt, Germany). Gene expression profiles were compared at indicated time points after stimulation with TGF-beta (1 ng/ml) using the Human Gene 1.0 ST arrays (Affymetrix). In total 18 hybridizations are included in this series.
Publication Title
TGF-β stimulation in human and murine cells reveals commonly affected biological processes and pathways at transcription level.
Sample Metadata Fields
Specimen part, Cell line, Time
View Samples- Mus musculus
- 12 Downloadable Samples
- Affymetrix Mouse Gene 1.0 ST Array (mogene10st)
Description
We here compared gene expression profiles of primary murine hepatocytes (mPC) upon stimulation with 1 ng/ml TGF-beta1 for 20 min, 2 hours and 4 hours with untreated cells. Experiments were done in three independent replicates. The goal of this study was to determine genes regulated by TGF-beta1.
Publication Title
TGF-β stimulation in human and murine cells reveals commonly affected biological processes and pathways at transcription level.
Sample Metadata Fields
Sex, Specimen part, Time
View Samples