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GSE108671
Mus musculus
15 Downloadable Samples
Affymetrix Mouse Gene 2.0 ST Array (mogene20st)
Description
This SuperSeries is composed of the SubSeries listed below.
Publication Title
Telmisartan Protects a Microglia Cell Line from LPS Injury Beyond AT1 Receptor Blockade or PPARγ Activation.
Sample Metadata Fields
Specimen part, Cell line, Treatment
View Samples- Mus musculus
- 12 Downloadable Samples
- Affymetrix Mouse Gene 2.0 ST Array (mogene20st)
Description
LPS and Telmisartan co-treatment of microglial BV2 cells.
Publication Title
Telmisartan Protects a Microglia Cell Line from LPS Injury Beyond AT1 Receptor Blockade or PPARγ Activation.
Sample Metadata Fields
Specimen part, Cell line, Treatment
View Samples- Mus musculus
- 3 Downloadable Samples
- Affymetrix Mouse Gene 2.0 ST Array (mogene20st)
Description
LPS, Telmisartan and GW9662 co-treatment of microglial BV2 cells.
Publication Title
Telmisartan Protects a Microglia Cell Line from LPS Injury Beyond AT1 Receptor Blockade or PPARγ Activation.
Sample Metadata Fields
Specimen part, Cell line, Treatment
View Samples- Mus musculus
- 24 Downloadable Samples
- Affymetrix Mouse Genome 430 2.0 Array (mouse4302)
Description
Neuroprotective therapies for retinal degeneration may be used to rescue retinal cells and preserve vision. Hypoxic preconditioning stabilizes the transcription factor HIF-1 in the retina and strongly protects photoreceptors in an animal model of light-induced retinal degeneration.
Publication Title
Analysis of the retinal gene expression profile after hypoxic preconditioning identifies candidate genes for neuroprotection.
Sample Metadata Fields
No sample metadata fields
View Samples- Mus musculus
- 4 Downloadable Samples
- Affymetrix Mouse Genome 430 2.0 Array (mouse4302)
Description
Aims: Resident cardiac progenitor cells show homing properties when injected into the injured but not into the healthy myocardium. The molecular background behind this difference in behavior needs to be studied to elucidate how adult progenitor cells can restore cardiac function of the damaged myocardium. Since the brain-derived neurotrophic factor (BDNF) moderates cardioprotection in injured hearts, we focused on delineating its regulatory role in the damaged myocardium.
Publication Title
Brain derived neurotrophic factor contributes to the cardiogenic potential of adult resident progenitor cells in failing murine heart.
Sample Metadata Fields
Age, Specimen part, Disease, Disease stage
View Samples- Mus musculus
- 10 Downloadable Samples
Illumina HiSeq 2000
Description
Clonal cellular variance often confounds reproducibility of forward and reverse genetic studies. We developed combinatorial approaches for whole genome saturated mutagenesis using haploid murine ES cells to permit induction and reversion of genetic mutations. Using these systems, we created a biobank with over 100000 individual ES cell lines with repairable and genetically bar coded mutations targeting 16950 genes. This biobank termed “Haplobank” is freely available. In addition, we developed a genetic color coding system for rapid repair of mutations and direct functional validation in sister clones. Using this system, we report functional validation of essential ES cell genes. We also identified phospholipase16G as a key pathway for cytotoxicity of human rhinoviruses, the most frequent cause of the common cold. Moreover, we derived 3D blood vessel organoids from haploid ES cells, combining conditional mutagenesis in haploid ES cells with tissue engineering. We identified multiple novel genes, such as Connexin43/Gja1, in blood vessel formation and tip cell specification in vitro and also in vivo. Taken together, we develop a conditional homozygous ES cell resource for the community to empower controlled genetic studies in murine ES cells and tissues derived from it. Overall design: RNA-Seq was carried out using standard protocols. https://www.haplobank.at/ecommerce/control/haplobank_resource
Publication Title
Comparative glycoproteomics of stem cells identifies new players in ricin toxicity.
Sample Metadata Fields
Subject
View Samples- Mus musculus
- 47 Downloadable Samples
- Ion Torrent Proton
Description
We induced mouse embryonic stem cells (ESCs) into B progenitors in in vitro culture. We previously reported that B cells derived from extra-embryonic yolks sac (YS) belong to innate-like B-1 cells, not conventional B-2 cells. Since ES cell differentiation into Blood lineage, it recapitulates YS hematopoiesis, we hypothesized that B cells produced by mouse ESCs belong to B-1 cells as well. We transplanted ESC-derived B-progenitor cells into immunodeficient mice and confirmed that ES-derived B cells differentiate into only B-1 and marginal zone B cells, not B-2 cells in vivo. We preformed gene expression profiles by RNA sequencing comparing ESC-derived, YS-derived, fetal liver derived, and adult bone marrow derived B progenitor cells to see their characteristics. Overall design: We compared gene expression profllings among B-1 progeniotors derived from ES, Yolk sac, and fetal liver, and B-2 progenitors from adult bone marrow. We isolated CD19+B220+ B-progenitor cells obtained from in vitro culture of mouse ES cells, yolk sac, and fetal liver (all B-1 biased) and bone marrow (B-2 biased) and performed RNA sequencing Please note that Flk1 is a marker of mesoderm that differentiate into endothelial cells and blood cells and VEcad (VE-cadherin) is a marker of endothelial cells. It is known that all hematopoietic cells are derived from lateral mesoderm (Flk1+) cells via endothelial phenotype (VE-cad+). Therefore, we differentiated ESCs into Flk1+ mesoderm or VEcad+ endothelial cells and isolated them by sorting (as indicated in the sample source name field), and replated them onto OP9-stromal cells that support B cell development.
Publication Title
Long-Term Engraftment of ESC-Derived B-1 Progenitor Cells Supports HSC-Independent Lymphopoiesis.
Sample Metadata Fields
Specimen part, Subject
View Samples- Mus musculus
- 20 Downloadable Samples
- Affymetrix Mouse Genome 430 2.0 Array (mouse4302)
Description
The E2F family consists of transcriptional repressors and activators that control cell proliferation. In the classic paradigm of cell cycle regulation, the three activators, E2F1, E2F2 and E2F3, are invariably depicted as the final components of a CDK/Rb signaling cascade that executes the transcriptional program necessary to commit cells to enter S phase.
Publication Title
Cell proliferation in the absence of E2F1-3.
Sample Metadata Fields
Specimen part
View Samples- Mus musculus
- 52 Downloadable Samples
- Illumina HiSeq 2500
Description
Large numbers of ribonucleotides are incorporated into the eukaryotic nuclear genome during S-phase due to imperfect discrimination against ribonucleoside triphosphates by the replicative DNA polymerases. Ribonucleotides, by far the most common DNA lesion in replicating cells, destabilize the DNA, and an evolutionarily conserved DNA repair machinery, ribonucleotide excision repair (RER), ensures ribonucleotide removal. Complete lack of RER is embryonically lethal. Partial loss-of-function mutations in the genes encoding subunits of RNase H2, the enzyme essential for initiation of RER, cause the SLE-related type I interferonopathy Aicardi-Goutières syndrome. Here we establish that selective inactivation of RER in mouse epidermis results in spontaneous DNA damage, epidermal hyperproliferation associated with loss of hair follicle stem cells and hair follicle function. The animals develop keratinocyte intraepithelial neoplasia and invasive squamous cell carcinoma with complete penetrance, despite potent type I interferon production and skin inflammation. Compromised RER-mediated genome maintenance might represent an important tumor-promoting principle in human cancer. Overall design: CD45+ CD49f- cells were were isolated from skin cell suspensions by FACS. Total RNA was isolated using the RNeasy Micro Kit+ (Qiagen). mRNA libraries were prepared using a SMART protocol and subjected to deep sequencing on an Illumina®HiSeq 2500.
Publication Title
Ribonucleotide Excision Repair Is Essential to Prevent Squamous Cell Carcinoma of the Skin.
Sample Metadata Fields
Specimen part, Subject
View Samples- Mus musculus
- 24 Downloadable Samples
- Illumina HiSeq 2500
Description
Large numbers of ribonucleotides are incorporated into the eukaryotic nuclear genome during S-phase due to imperfect discrimination against ribonucleoside triphosphates by the replicative DNA polymerases. Ribonucleotides, by far the most common DNA lesion in replicating cells, destabilize the DNA, and an evolutionarily conserved DNA repair machinery, ribonucleotide excision repair (RER), ensures ribonucleotide removal. Complete lack of RER is embryonically lethal. Partial loss-of-function mutations in the genes encoding subunits of RNase H2, the enzyme essential for initiation of RER, cause the SLE-related type I interferonopathy Aicardi-Goutières syndrome. Here we establish that selective inactivation of RER in mouse epidermis results in spontaneous DNA damage, epidermal hyperproliferation associated with loss of hair follicle stem cells and hair follicle function. The animals develop keratinocyte intraepithelial neoplasia and invasive squamous cell carcinoma with complete penetrance, despite potent type I interferon production and skin inflammation. Compromised RER-mediated genome maintenance might represent an important tumor-promoting principle in human cancer. Overall design: Keratinocytes (CD49f+) cells were isolated from skin cell suspensions by FACS. Total RNA was isolated using the RNeasy Mini Kit+ (Qiagen). mRNA libraries were prepared and subjected to deep sequencing on an Illumina®HiSeq.
Publication Title
Ribonucleotide Excision Repair Is Essential to Prevent Squamous Cell Carcinoma of the Skin.
Sample Metadata Fields
Specimen part, Subject
View Samples