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GSE46511
Mus musculus
8 Downloadable Samples
Affymetrix Mouse Genome 430 2.0 Array (mouse4302)
Description
NIH3T3 in the middle of G0 to G1 transion consists of the cells which is still staying G0 phase and the cells which enters G1. Monitoring the expressions of p27 and Cdt1 enables to distinguish these two; p27+/Cdt1+ cells as the cells in G0 phase and p27-Cdt1+ cells as G1 phase
Publication Title
A novel cell-cycle-indicator, mVenus-p27K-, identifies quiescent cells and visualizes G0-G1 transition.
Sample Metadata Fields
Cell line
View Samples- Mus musculus
- 6 Downloadable Samples
Illumina HiSeq 2000
Description
Bone marrow mesenchymal stromal cells (MSCs) that express high levels of stem cell factor (SCF) and CXC chemokine ligand 12 (CXCL12) are one crucial component of the hematopoietic stem cell (HSC) niche. While the secreted factors produced by MSCs to support HSCs have been well described, little is known regarding the transcriptional regulators controlling the cell fate of MSCs and thus indirectly maintaining HSCs. Bmi1 is a polycomb group protein that regulates HSCs both cell intrinsically and extrinsically, but it is unknown in which cell type and how Bmi1 functions to maintain HSCs extrinsically. Here we show that Bmi1 maintains HSCs by preventing adipogenic differentiation of MSCs. Bmi1 is highly expressed in MSCs but becomes downregulated upon adipogenic differentiation and during aging. Deleting Bmi1 from MSCs increased marrow adipocytes, induced HSC quiescence and depletion, and impaired hematopoiesis. We found that Bmi1 repressed multiple developmental programs in MSCs by safeguarding the repressive epigenetic marks histone H2A ubiquitylation and H3 lysine 27 trimethylation. We identified a novel adipogenic program governed by Pax3, which Bmi1 repressed in MSCs. Our results establish Bmi1 as a critical regulator of MSC cell fate that suppresses marrow adipogenesis to create a supportive niche for HSCs. Overall design: RNA-Seq of two treatments (Ctrl, KO) with three replications per treatment.
Publication Title
Bmi1 Suppresses Adipogenesis in the Hematopoietic Stem Cell Niche.
Sample Metadata Fields
Specimen part, Subject
View Samples- Mus musculus
- 19 Downloadable Samples
- Affymetrix Mouse Genome 430 2.0 Array (mouse4302)
Description
We found that a number of Tfh cells downmodulated BCL6 protein after their development, and we sought to compare the gene expression between BCL6-hi Tfh cells and BCL6-low Tfh cells.
Publication Title
Bcl6 protein expression shapes pre-germinal center B cell dynamics and follicular helper T cell heterogeneity.
Sample Metadata Fields
Specimen part
View Samples- Homo sapiens
- 5 Downloadable Samples
- Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
Treatment of MCF7 breast cancer cells by cisplatin leads to a very specific metabolic response and an onset of cell death about 10-11 h after beginning of treatment. For more detailed understanding of the molecular processes underlying the specific metabolic response, mRNA was isolated from MCF7 cells when the specific changes, (i) induction of glycolysis and (ii) onset of cell death, were detected during online measurement in the cell biosensor system.
Publication Title
Real-time monitoring of cisplatin-induced cell death.
Sample Metadata Fields
Cell line
View Samples- Mus musculus
- 15 Downloadable Samples
- Illumina HiSeq 1000
Description
Specific deletion of suppressor of cytokine signaling 3 (Socs3) in keratinocytes can cause severe skin inflammation with infiltration of immune cells, however the molecular mechanisms and key regulatory pathways involved remains poorly understood. To investigate the role of Socs3 in keratinocytes, we generated and analyzed global RNA-Seq profiles in Socs3 conditional knockout (cKO) mice at two different stages (2- and 10- weeks). Over 400 shared genes were found to be significantly regulated at both time points. Two week samples were marked by initial skin barrier dysfunction established by the downregulation of keratin associated genes and upregulation of genes regulating lipid metabolism. Subsequent increase in expression level of multiple chemokines and cytokines at 10 week were observed representing response to skin inflammation caused by the disruption of skin barrier function. A group of activator protein-1 related genes were to found to be highly elevated in Socs3 cKO mice at both time points. This observation was duly validated using qRT-PCR in Socs3 depleted human keratinocyte–derived HaCaT cells. Overall this study reveals an important regulatory dynamics of Socs3 in skin barrier dysfunction. Overall design: Socs3 cKO mice mRNA profiles of 2 and 10 week wild type (WT) C57BL/6 mice were generated by sequencing using HiSeq 1000 system (Illumina) machine which could read a 50 bp sequence.
Publication Title
Insights into gene expression profiles induced by Socs3 depletion in keratinocytes.
Sample Metadata Fields
Age, Specimen part, Cell line, Subject
View Samples- Homo sapiens
- 7 Downloadable Samples
- Affymetrix Human Gene 1.0 ST Array (hugene10st)
Description
This SuperSeries is composed of the SubSeries listed below.
Publication Title
High-throughput screening of tyrosine kinase inhibitor cardiotoxicity with human induced pluripotent stem cells.
Sample Metadata Fields
Specimen part, Cell line, Treatment, Subject
View Samples- Homo sapiens
- 7 Downloadable Samples
- Affymetrix Human Gene 1.0 ST Array (hugene10st)
Description
Tyrosine kinase inhibitors (TKIs), despite efficacy as anti-cancer therapies, are associated with cardiovascular side effects ranging from induced arrhythmias to heart failure. We have utilized patient-specific human induced pluripotent stem cell-derived cardiomyocytes (hiPSC-CMs), generated from 11 healthy individuals and 2 patients receiving cancer treatment, to screen FDA-approved TKIs for cardiotoxicities by measuring alterations in cardiomyocyte viability, contractility, electrophysiology, calcium handling, and signaling. With these data, we generated a cardiac safety index to assess cardiotoxicities of existing TKIs. Many TKIs with a low cardiac safety index exhibit cardiotoxicity in patients. We also derived endothelial cells (hiPSC-ECs) and cardiac fibroblasts (hiPSC-CFs) to examine cell type-specific cardiotoxicities. Using high-throughput screening, we determined that VEGFR2/PDGFR-inhibiting TKIs caused cardiotoxicity in hiPSC-CMs, hiPSC-ECs, and hiPSC-CFs. Using phosphoprotein analysis, we determined that VEGFR2/PDGFR-inhibiting TKIs led to a compensatory increase in cardioprotective insulin and insulin-like growth factor (IGF) signaling in hiPSC-CMs. Activating cardioprotective signaling with exogenous insulin or IGF1 improved hiPSC-CM viability during co-treatment with cardiotoxic VEGFR2/PDGFR-inhibiting TKIs. Thus, hiPSC-CMs can be used to screen for cardiovascular toxicities associated with anti-cancer TKIs, correlating with clinical phenotypes. This approach provides unexpected insights, as illustrated by our finding that toxicity can be alleviated via cardioprotective insulin/IGF signaling.
Publication Title
High-throughput screening of tyrosine kinase inhibitor cardiotoxicity with human induced pluripotent stem cells.
Sample Metadata Fields
Treatment, Subject
View Samples- Mus musculus
- 12 Downloadable Samples
- Affymetrix Mouse Gene 1.0 ST Array (mogene10st)
Description
The division rate of hematopoietic stem cells (HSCs) are promoted by estradiol. To identify the mechanism by which estradiol regulates HSCs, we performed gene expresssion profiling of HSCs isolated from mice of both sexes treated with either control vehicle (oil) or estradiol for one week.
Publication Title
Oestrogen increases haematopoietic stem-cell self-renewal in females and during pregnancy.
Sample Metadata Fields
Sex, Specimen part
View Samples- Homo sapiens
- 4 Downloadable Samples
- Illumina HiSeq 2500
Description
Analysis of whole gene expression during differentiation from hiPS cells into hepatocyte-like cells. The hypothesis tested in the present study was that the hepatocyte-like cells induced with adrenergic receptor agonists were identical to those induced with conventional growth factors (hepatocyte growth factor and oncostatin M). Results provide the important information of the differentiation mechanisms from hepatoblasts into hepatocytes. Overall design: Total RNA obtained from undifferentiated hiPS cells, hiPS cell-derived hepatoblast-like and hepatocyte-like cells. The hiPS cells were induced to differentiate into hepatoblast-like cells, then the cells were treated with methoxamine or growth factors (hepatocyte growth factor and oncostatin M) to induce the differentiation into hepatocyte-like cells.
Publication Title
Adrenergic receptor agonists induce the differentiation of pluripotent stem cell-derived hepatoblasts into hepatocyte-like cells.
Sample Metadata Fields
Sex, Cell line, Subject
View Samples- Mus musculus
- 10 Downloadable Samples
- Affymetrix Mouse Genome 430 2.0 Array (mouse4302)
Description
This SuperSeries is composed of the SubSeries listed below.
Publication Title
Tbx3-dependent amplifying stem cell progeny drives interfollicular epidermal expansion during pregnancy and regeneration.
Sample Metadata Fields
Sex, Specimen part
View Samples