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SRP102431
Mus musculus
9 Downloadable Samples
Ion Torrent Proton
Description
Analysis of murine cardiomyocyte cell line HL-1 treated with Ivermectin or Importazole. Results provide insight into the pathways regulated by the treatments. Overall design: RNA-seq of mouse HL-1 cardiomyocytes treated with vehicle (DMSO), Ivermectin, or Importazole for 24 hours, in triplicate, using Ion Proton System.
Publication Title
Antihypertrophic Effects of Small Molecules that Maintain Mitochondrial ATP Levels Under Hypoxia.
Sample Metadata Fields
Specimen part, Cell line, Treatment, Subject
View Samples- Mus musculus, Rattus norvegicus
- 53 Downloadable Samples
Affymetrix Mouse Genome 430 2.0 Array (mouse4302)
Description
This SuperSeries is composed of the SubSeries listed below.
Publication Title
Neuroprotective effects of brain-derived neurotrophic factor in rodent and primate models of Alzheimer's disease.
Sample Metadata Fields
Treatment
View Samples- Rattus norvegicus
- 27 Downloadable Samples
- Affymetrix Mouse Genome 430 2.0 Array (mouse4302)
Description
Patterns of gene expression in the aged entorhinal cortex and hippocampus were examined one month after entorhinal administration of BDNF lentivirus. Whole-genome patterns of expression were examined using Affymetrix arrays four weeks after entorhinal injection of lentiviral-BDNF or GFP injection compared to control subjects.
Publication Title
Neuroprotective effects of brain-derived neurotrophic factor in rodent and primate models of Alzheimer's disease.
Sample Metadata Fields
Treatment
View Samples- Homo sapiens
- 14 Downloadable Samples
Affymetrix Human Genome U133A 2.0 Array (hgu133a2)
Description
Nuclear FTY720-P is a potent inhibitor of class I histone deacetylases (HDACs) that enhances histone acetylations and regulates expression of a restricted set of genes independently of its known effects on canonical signaling through sphingosine-1-phosphate (S1P) receptors. We found that FTY720 is phosphorylated in Era-negative breast cancer cells by nuclear sphingosine kinase 2 and accumulates these cells.
Publication Title
The phosphorylated prodrug FTY720 is a histone deacetylase inhibitor that reactivates ERα expression and enhances hormonal therapy for breast cancer.
Sample Metadata Fields
Cell line
View Samples- Homo sapiens
- 10 Downloadable Samples
- Illumina HiSeq 2000
Description
Purpose: RNA-Seq analysis can help identify large set of differentially expressed genes at a time. We performed RNA-Seq analysis to identify differentially expressed genes in the PBMCs of war veterans suffering from PTSD. Methods: Total RNA from PBMCs from PTSD +ve and -ve individuals were used for RNA-Seq analysis. Results: We obtained, on average, ~60 millions reads per sample. More than 70% of the reads were mapped to human genome. Functional analysis of the differentially expressed genes (362) revealed dysregulation in immune system network. Conclusions: Our present study provides further proof that immune system related genes and pathways are dysregulated in PTSD PBMCs. Overall design: RNA-Seq was performed with RNA from 5 each control and PTSD individuals. PBMCs collected within one hour of blood draw were used for RNA isolation. 1 ug of total RNA was used for library synthesis and sequenced in a HighSeq 2000 illumina instrument at Tufts University.
Publication Title
Decreased AGO2 and DCR1 in PBMCs from War Veterans with PTSD leads to diminished miRNA resulting in elevated inflammation.
Sample Metadata Fields
Specimen part, Subject
View Samples- Mus musculus
- 8 Downloadable Samples
- Affymetrix Mouse Genome 430 2.0 Array (mouse4302)
Description
Identification of cancer stem/initiating cells (CSCs/CICs) by a specific marker is useful for diagnosis and therapy of cancer. We have determined that PSF1 which plays a role in DNA replication in lower species is strongly expressed in wide range of normal stem cell population. Here, utilizing the transcriptional activity of PSF1 promoter in tumor cell xenograft model, we show that PSF1high cancer cells display malignant features including high proliferating activity, serial transplantation potential, and metastatic ability those are used for criteria of CSCs/CICs. PSF1high cancer cells localize in perivascular region and genetically display ES cell like signature. Silencing of PSF1 by RNAi inhibited growth of cancer cells mediated by disruption of DNA synthesis and chromosomal segregation. These suggested that PSF1 is a possible maker and a molecular target of CSCs/CICs.
Publication Title
PSF1, a DNA replication factor expressed widely in stem and progenitor cells, drives tumorigenic and metastatic properties.
Sample Metadata Fields
Cell line
View Samples- Mus musculus
- 9 Downloadable Samples
- Affymetrix Mouse Gene 1.0 ST Array (mogene10st)
Description
G-CSF treatment targets CXCL12-abundant reticular (CAR) cells to suppress their production of a number of B trophic factors, including CXCL12, IL-6, IL-7, IGF-1, and Flt3 ligand.
Publication Title
Granulocyte colony-stimulating factor reprograms bone marrow stromal cells to actively suppress B lymphopoiesis in mice.
Sample Metadata Fields
Treatment
View Samples- Homo sapiens
- 12 Downloadable Samples
- Illumina HiSeq 1500
Description
Background: Blau syndrome, or early-onset sarcoidosis, is a juvenile-onset systemic granulomatosis associated with a mutation in Nucleotide-binding oligomerization domain 2 (NOD2). The underlying mechanisms of Blau syndrome leading to autoinflammation are still unclear, and there is currently no effective specific treatment for Blau syndrome. Objectives: To elucidate the mechanisms of autoinflammation in Blau syndrome, we sought to clarify the relation between disease associated-mutant NOD2 and the inflammatory response in human samples. Methods: Blau syndrome-specific induced pluripotent stem cells (iPSCs) lines were established. To precisely evaluate the in vitro phenotype of iPSC-derived cells, the disease-associated NOD2 mutation of iPSCs was corrected using a CRISPR/Cas9 system. We also introduced the same NOD2 mutation into a control iPSC line. These isogenic iPSCs were then differentiated into monocytic cell lineages, and the status of NF-?B pathway and proinflammatory cytokine secretion were investigated. Results: We focused on the signals that upregulate the expression of NOD2, especially IFN-? signaling. IFN-? treatment of NOD2-mutant macrophages induced ligand-independent NF-?B activation and proinflammatory cytokine production. IFN-? treatment acted as a priming signal through the up-regulation of NOD2 protein and recruitment of NOD2 on the basement membrane. Conversely, the production of proinflammatory cytokines by MDP, a ligand of NOD2, was decreased in mutant macrophages. Conclusions: Our data support the significance of ligand-independent autoinflammation in the pathophysiology of Blau syndrome. Our comprehensive isogenic disease-specific iPSC panel provides a useful platform for probing therapeutic and diagnostic clues for the treatment of Blau syndrome patients. Overall design: RNA-sequencing was conducted to identify the genes expressed in reponse to stimulation in different manners between WT and MT cells
Publication Title
Pluripotent stem cell models of Blau syndrome reveal an IFN-γ-dependent inflammatory response in macrophages.
Sample Metadata Fields
Specimen part, Disease, Disease stage, Subject
View Samples- Homo sapiens
- 8 Downloadable Samples
- Illumina HiSeq 2000
Description
We performed RNA-Seq on PHF21A-deficient patient-dervied lymphoblasts as well as two unaffected individuals. Overall design: We performed RNA-Seq from patient-derived lymphoblast cells. Libraries were polyA-selected and strand-specific according to the protocol described in PMID: 25607527
Publication Title
Transcriptome Analysis Revealed Impaired cAMP Responsiveness in PHF21A-Deficient Human Cells.
Sample Metadata Fields
Sex, Specimen part, Disease stage, Subject
View Samples- Homo sapiens
- 4 Downloadable Samples
- Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
We explored the functional role of YAP in SCLC cells (SBC3 and SBC5) by YAP knockdown.
Publication Title
YAP and TAZ modulate cell phenotype in a subset of small cell lung cancer.
Sample Metadata Fields
Cell line
View Samples