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GSE14561
Mus musculus
17 Downloadable Samples
Affymetrix Mouse Genome 430 2.0 Array (mouse4302)
Description
Somatic mutation in the X-linked phosphatidylinositol glycan class A (PIG-A) gene causes glycosylphosphatidylinositol (GPI) anchor deficiency in humans with Paroxysmal Nocturnal Hemoglobinuria (PNH). Clinically, patients with PNH have intravascular hemolysis, venous thrombosis and bone marrow failure. We produced a conditional Pig-a knock-out mouse model specifically inactivating the Pig-a gene in hematopoietic cells to study the role of PIG-A deficiency in PNH pathophysiology. We used Affymetrix Mouse Genome 430 2.0 chips to investigate the gene expression pattern in the mouse model of targeted Pig-a deletion.
Publication Title
Phenotypic and functional characterization of a mouse model of targeted Pig-a deletion in hematopoietic cells.
Sample Metadata Fields
No sample metadata fields
View Samples- Homo sapiens
- 33 Downloadable Samples
- Affymetrix Human Genome U133A 2.0 Array (hgu133a2)
Description
We performed microarray to compare gene expression patterns of PBMC treated with rATG or hATG. Fold changes were compared using 2-way ANOVA tests for untreated, rATG- and hATG-treated PBMC. In PBMC treated with 10 ug/mL rATG, compared with untreated PBMC, 478 genes showed up-regulation, and 341 genes showed down-regulation at 24 hours using 10% FDR and 2-fold change cutoff. Immediately striking was that 10 ug/mL hATG had affected many fewer genes than did rATG: only 3 genes were up-regulated and 6 genes were down-regulated at 24 hours in hATG-treated PBMC. When we compared rATG with hATG, rATG induced up-regulation of 268 genes and down-regulation of 95 genes. These genes belong to the categories of immune response (64 genes), cytokine-cytokine receptor interaction (36 genes), regulation of cell proliferation (24 genes), cell cycle (23 genes), cell growth (8 genes), apoptosis (7 genes), and others.
Publication Title
Rabbit ATG but not horse ATG promotes expansion of functional CD4+CD25highFOXP3+ regulatory T cells in vitro.
Sample Metadata Fields
No sample metadata fields
View Samples- Homo sapiens
- 9 Downloadable Samples
Illumina HiSeq 2500
Description
Purpose: Recurrent ASXL1 mutations are frequently observed in all spectrums of myeloid malignancies and published data suggests that ASXL1 mutations may be involved in leukemic transformation as a tumor suppressor. Yet the molecular mechanisms of cell desitiny regulated by ASXL1 are to be further delineated. Methods: mRNA profiles of wild-type (WT) and CRISPR/Cas9 induced ASXL1 mutated U937 cell lines were generated by next generation sequencing, using Illumina HiSeq2500. Sequence reads were trimmed to remove possible adapter sequences and nucleotides with poor quality at the ends. Remaining sequence reads were then aligned to the human reference genome (hg19) using Tophat2. Gene read counts were measured using FeatureCounts and FPKM values were calculated with cufflinks. edgeR was used to identify differentially expressed genes between conditions, and topGO was used for annotation (Alexa, Rahnenfuhrer, and Lengauer, 2006). Sample comparison for differential gene expression was as follows: WTblk and WT1 versus MT2, MT3, MT4, and MT5. Gene enrichment set analysis (GSEA) was conducted with KEGG, Biocarta, and Reactome pathway datasets (Subramanian et al., 2005). Results: ASXL1-mutated cells displayed impaired differentiation capacity. RNA-seq was used to compare transcriptomes of ASXL1-mutated and WT U937 cells. Transcriptom analysis revealed that ASXL1 mutations decreased the expression of genes essential to myeloid differentiation, including CYBB and CLEC5A genes, which manifested in ASXL1-MT U937 cells as perturbed potential of differentiation compared with WT cells. Also, gene set enrichment analysis revealed that ASXL1 mutations masively affected gene sets relating to cell death and survival. Conclusion: By introduction of mutations into genome using the CRISPR/Cas9 system, we established ASXL1-mutated U937 cell lines. Our results indicated that ASXL1 mutations perturbed monocytic/phagocyte differentiation, which is a hallmark of myeloid malignancies, by down regulating genes essential to myeloid differentiation, including CYBB and CLEC5A, also massively affected multiple gene sets involving in cell survival. Overall design: mRNA profiles of wild type (WT) and ASXL1 mutated U937 cell lines were generated by deep sequencing using Illumina HiSeq2500
Publication Title
CRISPR/Cas9-mediated ASXL1 mutations in U937 cells disrupt myeloid differentiation.
Sample Metadata Fields
Specimen part, Cell line, Subject
View Samples- Homo sapiens
- 17 Downloadable Samples
- Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
B19V NS1 is known to be cytotoxic and involved in the pathogenesis of B19V infection. Our previous data demonstrated that NS1 impaired the cell-cycle progression of the CD36+ EPCs by inducing a stable G2 arrest. Microarray analysis was used to identify genes whose expressions were associated with the NS1-induced G2 arrest. A total of 1045 genes displayed a more than 1.5-fold differential expression in the NS1-transduced cells. Out of 1045 differentially expressed genes, 177 were involved in cell-cycle regulation and 51 were involved in the regulation of cell differentiation.
Publication Title
Human parvovirus B19 causes cell cycle arrest of human erythroid progenitors via deregulation of the E2F family of transcription factors.
Sample Metadata Fields
Specimen part
View Samples- Homo sapiens
- 12 Downloadable Samples
- Illumina HiSeq 2500
Description
Purpose: DNA methyltransferase 3A (DNMT3A) mediates de novo DNA methylation. Mutations in DNMT3A are associated with hematological malignancies, most frequently acute myeloid leukemia. DNMT3A mutations are hypothesized to establish a pre-leukemic state, rendering cells vulnerable to secondary oncogenic mutations and malignant transformation. However, the mechanisms by which DNMT3A mutations contribute to leukemogenesis are not well-defined. Methods: mRNA profiles of wild-type (WT) and DNMT3A mutated k562 cell lines were generated by deep sequencing, using Illumina HiSeq2500. Sequence reads were trimmed to remove possible adapter sequences and nucleotides with poor quality at the ends. Remaining sequence reads were then aligned to the human reference genome (hg19) using Tophat2. Gene read counts were measured using FeatureCounts and FPKM values were calculated with cufflinks. edgeR was used to identify differentially expressed genes between conditions, and topGO was used for annotation (Alexa, Rahnenfuhrer, and Lengauer, 2006). Sample comparison for differential gene expression was as follows: WTblk and WT1 versus MT2, MT3, MT4, and MT5. Gene enrichment set analysis (GSEA) was conducted with KEGG, Biocarta, and Reactome pathway datasets (Subramanian et al., 2005). Results: DNMT3A-mutated cells displayed impaired differentiation capacity. RNA-seq was used to compare transcriptomes of DNMT3A-mutated and WT cells; DNMT3A ablation resulted in downregulation of genes involved in spliceosome function, causing dysfunction of RNA splicing. Unexpectedly, we observed DNMT3A-mutated cells to exhibit marked genomic instability and an impaired DNA damage response compared to WT. Conclusions: CRISPR/Cas9-mediated DNMT3A-mutated K562 cells may be used to model effects of DNMT3A mutations in human cells. Our findings implicate aberrant splicing and induction of genomic instability as potential mechanisms by which DNMT3A mutations might predispose to malignancy. Overall design: mRNA profiles of wild type (WT) and DNMT3A mutated K562 cell lines were generated by deep sequencing using Illumina HiSeq2500
Publication Title
Abnormal RNA splicing and genomic instability after induction of DNMT3A mutations by CRISPR/Cas9 gene editing.
Sample Metadata Fields
Specimen part, Cell line, Subject
View Samples- Mus musculus
- 2 Downloadable Samples
- Illumina HiSeq 2000
Description
Long-term survival and antitumor immunity of adoptively transferred CD8+ T cells is dependent on their metabolic fitness, but approaches to isolate therapeutic T cells based on metabolic features are not well established. Here we utilized a lipophilic cationic dye tetramethylrhodamine methyl ester (TMRM) to identify and isolate metabolically robust T cells based on their mitochondrial membrane potential (??m). Comprehensive metabolomic and gene expression profiling demonstrated global features of improved metabolic fitness in low-??m-sorted CD8+ T cells. Transfer of these low-??m T cells was associated with superior long-term in vivo persistence and an enhanced capacity to eradicate established tumors compared with high-??m cells. Use of ??m-based sorting to enrich for cells with superior metabolic features was observed in CD8+, CD4+ T cell subsets, and long-term hematopoietic stem cells. This metabolism-based approach to cell selection may be broadly applicable to therapies involving the transfer of HSC or lymphocytes for the treatment of viral-associated illnesses and cancer. Overall design: mRNA-Sequencing of gene expression profiles in mouse CD8 cells (TMRM high and TMRM low).
Publication Title
Mitochondrial Membrane Potential Identifies Cells with Enhanced Stemness for Cellular Therapy.
Sample Metadata Fields
Specimen part, Cell line, Subject
View Samples- Mus musculus
- 9 Downloadable Samples
- Illumina HiSeq 2000
Description
Canonical WNT-signaling is essential for placode formation irrespective of appendage type. At sites of placode initiation, Although WNT-signaling occurs in both epithelium and mesenchyme, the site of most intense activity as revealed by the WNT reporter Axin2-LacZ was in a zone just below the epithelial-mesenchymal interface. In ventral foot-skin, this WNT activity peaked at E17.5, concomitant with sweat bud fate commitment, while in dorsal back-skin, it began at E14.5, concomitant with HF fate specification. Overall design: To address whether WNT-signaling within this zone might regionally influence the transcriptional landscape of body-site mesenchymes to support distinct epithelial fates, we transcriptionally profiled the Axin2-positive and Axin2-negative dermal cells following their FACS-purification from E17.5 ventral foot-skin and E14.5 dorsal back-skin
Publication Title
Spatiotemporal antagonism in mesenchymal-epithelial signaling in sweat versus hair fate decision.
Sample Metadata Fields
Specimen part, Subject
View Samples- Mus musculus
- 18 Downloadable Samples
- Illumina HiSeq 2000
Description
After characterizing super-enhancer-associated chromatin dynamics accompanied by malignant progression of skin stem cells, we show that ETS family members auto-regulate themselves and a cohort of cancer-associated super-enhancer transcription factors which together are essential for tumor maintenance. Overall design: Epidermal basal stem cells from ETS2(T72D) super-activated epidermis and normal epidermis were FACS-prufied for RNA-sequencing.
Publication Title
ETS family transcriptional regulators drive chromatin dynamics and malignancy in squamous cell carcinomas.
Sample Metadata Fields
Sex, Specimen part, Cell line, Subject
View Samples- Mus musculus
- 9 Downloadable Samples
- Illumina HiSeq 2000
Description
After characterizing super-enhancer-associated chromatin dynamics accompanied by malignant progression of skin stem cells, we show that ETS family members auto-regulate themselves and a cohort of cancer-associated super-enhancer transcription factors which together are essential for tumor maintenance. Overall design: Mouse skin squamouse cell carcinoma (SCC) tumor-initiating stem cells (SCC-SC), hair follicle stem cells (HF-SC) and epidermal stem cells (Epi-SC) were FACS-prufied for RNA-sequencing.
Publication Title
ETS family transcriptional regulators drive chromatin dynamics and malignancy in squamous cell carcinomas.
Sample Metadata Fields
Sex, Cell line, Subject
View Samples- Mus musculus
- 8 Downloadable Samples
- Illumina HiSeq 2000
Description
We performed RNA_Seq on purified hair follicle stem cells (HFSCs)and their direct progenty, transit amplifying cells (TACs) using temorally and spatially regulated Cre lines. Overall design: Consequences of loss of Bmpr1a in either HFSC (K15-CrePGR;Bmpr1a fl/fl), or TACs (1. Shh-CreER:Bmpr1a fl/fl or 2. K15-CrePGR;Bmpr1a fl/fl derived)
Publication Title
BMP signaling and its pSMAD1/5 target genes differentially regulate hair follicle stem cell lineages.
Sample Metadata Fields
No sample metadata fields
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