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GSE42253
Homo sapiens
6 Downloadable Samples
Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
Hsp90 is critical for regulation of the phenotype and functional activity of human T lymphocytes and natural killer (NK) cells.
Publication Title
Heat shock protein 90 is critical for regulation of phenotype and functional activity of human T lymphocytes and NK cells.
Sample Metadata Fields
Specimen part, Treatment
View Samples- Mus musculus
- 49 Downloadable Samples
NextSeq 500
Description
Reprogram-Seq leverages organ-specific cell atlas data with single-cell perturbation and computational analysis to predict, evaluate, and optimize TF combinations that reprogram a cell type of interest. Overall design: Focusing on the cardiac system, we performed Reprogram-Seq on P0 mouse heart cells to generate a reference transcriptomic map. Based on the reference map, we selected TF candidates and tests 1000s of TF cocktails for direct lineage conversion by scRNA-Seq.
Publication Title
Rational Reprogramming of Cellular States by Combinatorial Perturbation.
Sample Metadata Fields
Specimen part, Subject
View Samples- Mus musculus
- 36 Downloadable Samples
- NextSeq 500
Description
Reprogram-Seq leverages organ-specific cell atlas data with single-cell perturbation and computational analysis to predict, evaluate, and optimize TF combinations that reprogram a cell type of interest. Overall design: Focusing on the cardiac system, we performed Reprogram-Seq on P0 mouse heart cells to generate a reference transcriptomic map. Based on the reference map, we selected TF candidates and tests 1000s of TF cocktails for direct lineage conversion by scRNA-Seq.
Publication Title
Rational Reprogramming of Cellular States by Combinatorial Perturbation.
Sample Metadata Fields
Specimen part, Subject
View Samples- Mus musculus
- 7 Downloadable Samples
- NextSeq 500
Description
Reprogram-Seq leverages organ-specific cell atlas data with single-cell perturbation and computational analysis to predict, evaluate, and optimize TF combinations that reprogram a cell type of interest. Overall design: Focusing on the cardiac system, we performed Reprogram-Seq on P0 mouse heart cells to generate a reference transcriptomic map. Based on the reference map, we selected TF candidates and tests 1000s of TF cocktails for direct lineage conversion by scRNA-Seq. This series includes uninfected, non-transformed MEFs.
Publication Title
Rational Reprogramming of Cellular States by Combinatorial Perturbation.
Sample Metadata Fields
Specimen part, Subject
View Samples- Mus musculus
- 1 Downloadable Sample
- NextSeq 500
Description
Reprogram-Seq leverages organ-specific cell atlas data with single-cell perturbation and computational analysis to predict, evaluate, and optimize TF combinations that reprogram a cell type of interest. Overall design: Focusing on the cardiac system, we performed Reprogram-Seq on P0 mouse heart cells to generate a reference transcriptomic map. Based on the reference map, we selected TF candidates and tests 1000s of TF cocktails for direct lineage conversion by scRNA-Seq.
Publication Title
Rational Reprogramming of Cellular States by Combinatorial Perturbation.
Sample Metadata Fields
Specimen part, Subject
View Samples- Mus musculus
- 1 Downloadable Sample
- NextSeq 500
Description
Reprogram-Seq leverages organ-specific cell atlas data with single-cell perturbation and computational analysis to predict, evaluate, and optimize TF combinations that reprogram a cell type of interest. Overall design: Focusing on the cardiac system, we performed Reprogram-Seq on P0 mouse heart cells to generate a reference transcriptomic map. Based on the reference map, we selected TF candidates and tests 1000s of TF cocktails for direct lineage conversion by scRNA-Seq. This series includes reprogrammed MEFs with Myod1, day 7.
Publication Title
Rational Reprogramming of Cellular States by Combinatorial Perturbation.
Sample Metadata Fields
Specimen part, Cell line, Subject
View Samples- Mus musculus
- 1 Downloadable Sample
- NextSeq 500
Description
Reprogram-Seq leverages organ-specific cell atlas data with single-cell perturbation and computational analysis to predict, evaluate, and optimize TF combinations that reprogram a cell type of interest. Overall design: Focusing on the cardiac system, we performed Reprogram-Seq on P0 mouse heart cells to generate a reference transcriptomic map. Based on the reference map, we selected TF candidates and tests 1000s of TF cocktails for direct lineage conversion by scRNA-Seq.
Publication Title
Rational Reprogramming of Cellular States by Combinatorial Perturbation.
Sample Metadata Fields
Specimen part, Subject
View Samples- Mus musculus
- 1 Downloadable Sample
- NextSeq 500
Description
Gjd3-CreEGFP mice is a novel genetic tool to study the structural and molecular signatures of Atrioventricular Node (AVN) at a high resolution. Overall design: Focusing on the cardiac conduction system, we developed and rigorously characterized a geentic tool Gjd3-CreEGFP to perform in-depth analysis of AVN structure and composition. Utilizing this AVN-specific mouse model, we performed scRNA-Seq on neonatal Gjd3-CreEGFP mice to guide our single-cell atlas of the Atrio-ventricular conduction system (AVCS).
Publication Title
Using Gjd3-CreEGFP mice to examine atrioventricular node morphology and composition.
Sample Metadata Fields
Specimen part, Subject
View Samples- Mus musculus
- 15 Downloadable Samples
- Affymetrix Murine Genome U74A Version 2 Array (mgu74av2)
Description
We have previously demonstrated that bone marrow-derived DC can prevent diabetes development and halt progression of insulitis in NOD mice, the mouse model of type 1 diabetes (T1D). The DC population that was most effective in this therapy had a mature phenotype, expressed high levels of costimulatory molecules and secreted low levels of IL-12p70. The protective DC therapy induced regulatory Th2 cells that shifted the dominant Th1 environment, present in NOD mice, to a mixed Th1/Th2 milieu. Microarray analysis of therapeutic and non-therapeutic DC populations revealed several novel molecules that could play important roles in the observed DC-mediated therapy. The therapeutic DC population expressed a unique pattern of costimulatory molecules and chemokines, which were confirmed by flow cytometry and ELISA assays. We have performed in vitro chemotaxis assays that demonstrated the therapeutic DC preferentially attracted Th2 cells, as compared to Th1, Treg or nave T cells. In addition we quantified the in vivo migration of activated islet-specific T cells to the pancreas using novel cell labeling techniques and 19F nuclear magnetic resonance. A subcutaenous injection of therapeutic DC alters the migration of both Th1 and Th2 cells to the pancreas, and Th1 cells appeared in the lymph node draining the site of DC injection. These results suggest that the therapeutic function of DC is mediated in part by the chemoattractive properties of these DC for diabetogenic Th1 cells.
Publication Title
Gene expression analysis of dendritic cells that prevent diabetes in NOD mice: analysis of chemokines and costimulatory molecules.
Sample Metadata Fields
Sex
View Samples- Homo sapiens
- 12 Downloadable Samples
- Illumina HiSeq 2000
Description
There is some emerging evidence that members of the Schlafen (SLFN) family of proteins mediate antineoplastic responses, but the mechanisms accounting for these effects are not known. We provide evidence that human SLFN5, an interferon (IFN)- inducible member of the family, exhibits key roles in controlling motility and invasiveness of renal cell carcinoma (RCC) cells. Our studies define the mechanism by which this occurs, demonstrating that SLFN5 negatively controls expression of matrix metalloproteinases (MMP)-1 and -13 and several other genes involved in the control of malignant cell motility. Importantly, our data establish that SLFN5 expression correlates with a better overall survival in a large cohort of patients with RCC. The inverse relationship between SLFN5 expression and RCC aggressiveness raises the possibility of developing unique therapeutic approaches in the treatment of RCC, by modulating SLFN5 expression. Overall design: Examination of 2 SLFN5 knockdown cells and 2 controls, in triplicate.
Publication Title
Human Schlafen 5 (SLFN5) Is a Regulator of Motility and Invasiveness of Renal Cell Carcinoma Cells.
Sample Metadata Fields
No sample metadata fields
View Samples