Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1061334 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR27432792_1.fastq.gz | Fastqsanger.gz | |||
| SRR27432792_2.fastq.gz | Fastqsanger.gz | |||
| SRR27432793_1.fastq.gz | Fastqsanger.gz | |||
| SRR27432793_2.fastq.gz | Fastqsanger.gz | |||
| SRR27432794_1.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 16 |
Similar Datasets
Project description:To clarify the selective advantage of the GPI-AP- cells in paroxysmal nocturnal hemoglobinuria (PNH) patients, RNA-seq was applied to examine functional effects of the PIG-A mutation in human granulocytes.
2016-04-09 | GSE80062 | GEO
Project description:We performed single cell RNA sequencing of bone marrow samples (sorted Lineage+ cells, and sorted Lin-CD34+ HSPCs) from 8 patients with paroxysmal nocturnal hemoglobinuria (PNH) to understand PNH pathophysiology at high multi-dimensional resolution.
2026-03-10 | GSE248025 | GEO
Project description:Hierarchical Clonal Architecture In Paroxysmal Nocturnal Hemoglobinuria: Stepwise Acquisition of Mutations
| PRJNA254174 | ENA
Project description:T cells from paroxysmal nocturnal hemoglobinuria patients show an altered TNFR signaling pathway
| PRJNA327044 | ENA
Project 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. Keywords: Gene expression comparison between untransplanted and transplanted GPI-deficient bone marrow cells
2009-09-10 | GSE14561 | GEO
Project description:Overexpression of high mobility group AT-hook 2 (HMGA2) associated with truncations of its 3’ untranslated region (UTR) with let-7 micro RNA-complementary sequences have been identified in patients with paroxysmal nocturnal hemoglobinuria (PNH). Here, we generated transgenic mice (∆Hmga2 mice) with a 3’UTR-trncated Hmga2 cDNA that overexpress Hmga2 mRNA and protein in hematopoietic organs. ∆Hmga2 mice showed proliferative hematopoiesis that mimicked a myeloproliferative neoplasm (MPN)-like phenotype with increased numbers of all lineages of peripheral blood cells, hypercellular bone marrow (BM), splenomegaly with extramedullary erythropoiesis, and erythropoietin-independent erythroid colony formation compared to wild-type mice. ∆Hmga2 BM-derived cells took over most of hematopoiesis in competitive repopulations during serial BM transplants. When we bred mice with circulating PNH cells (Piga- mice) with ∆Hmga2 mice, the lack of GPI-linked proteins did not add an additional clonal advantage to the ∆Hmga2+ cells. In summary, our results showed that the overexpression of a 3’UTR-truncated Hmga2 leads to a proliferative hematopoiesis with clonal advantage, which may explain clonal expansion in PNH or MPN at the level of HSC. Eight independent preparations of RNA, which included each 2 samples of KLS cells and MEP cells from ∆Hmga2 mice and 2 each from WT mice. Each preparation was made from 4 or 6 mice.
2011-02-06 | E-GEOD-24071 | biostudies-arrayexpress
Project description:Purpose: to detect the expression differences of Long chain non coding RNA(Lnc RNA) in exosomes derived from Thrombus-derived exosomes in AMI patients, healthy human serum-source exosomes and AMI patients serum-source exosomes. Methods: Total RNA containing Long chain non coding RNA was extracted from Thrombus-derived exosomes in AMI patients. Use Agilent lncRNA array for lncRNA analysis. Each lncRNA was repeatedly detected by the probe 30 times. The array also contains 2164 Agilent control probes. Agilent Feature Extraction (Agilent) was used to analyze the lncRNA array data for data aggregation, standardization and quality control. Perform the default 90th percentile normalization method for date preprocessing. To select differentially expressed genes, we used thresholds of ≥2 and ≤−2 fold change, and the Benjamini-Hochberg corrected p vlaue was 0.05. Results: Compared with the Normal group, there were 2148 lncRNAs up-regulated and 2415 lncRNAs down-regulated in the serum group, and 2615 lncRNAs up-regulated and 452 lncRNAs down-regulated in the thrombus group. Compared with the serum group, there were 1374 lncRNAs up-regulated and 1218 lncRNAs down-regulated in the thrombus group. Conclusion: The 2615 lncRNAs upregulated relative to the Noormal group are candidates for regulatory targets of thrombosis-related regulatory pathways.
2025-02-14 | GSE213115 | GEO
Project description:In recent years, a critical clinical problem that cannot be ignored is the incidence of venous thrombosis gradually increasing. Although many animal models of thrombosis have been established, the complex mechanism of thrombosis has not been elucidated. We successfully established a new animal model of venous thrombosis by infrared-pulse laser selectively targeting damage to the venous endothelium of zebrafish tail, resulting in the aggregation of red blood cells and platelets at the site of injury, forming a thrombus, like the formation of thrombi caused by damaged human venous endothelium. o-Dianisidine staining showed increased hemoglobin density at the injury site and decreased hemoglobin density at the heart site. Utilizing laser microdissection technology, we targeted the acquisition of localized thrombus cell clusters for high-throughput transcriptome sequencing. The data were further analyzed through gene set variation analysis (GSVA) and gene set enrichment analysis (GSEA), with the transcriptome data being examined against backgrounds of GO, KEGG, Reactome, and WP databases. Combining these analyses with molecular biology techniques such as RT-qPCR, WISH, and Western Blot, we observed that, compared to the normal group, macrophages were activated, and erythrocyte differentiation was more vigorous post-thrombus formation. Signaling pathways related to cell adhesion and leukocyte migration were activated, and the expression of inflammatory cytokines increased. Notably, IL-6 and TNF-α significantly increased at the thrombus site, while other cytokines such as IL-1β, IL-10, P-selectin, STAT3, phosphorylated STAT3, p65, and phosphorylated p65 were major players in the inflammatory response during venous thrombosis. The venous thrombosis model established in this study allows a high degree of visualization of thrombosis and provides a feasible and powerful protocol for studying the mechanism of thrombosis. This study may serve as a new venous thrombosis model for exploring the detailed kinetics and underlying mechanisms of thrombosis formation.
2025-10-31 | GSE309638 | GEO
Project description:Overexpression of high mobility group AT-hook 2 (HMGA2) associated with truncations of its 3’ untranslated region (UTR) with let-7 micro RNA-complementary sequences have been identified in patients with paroxysmal nocturnal hemoglobinuria (PNH). Here, we generated transgenic mice (∆Hmga2 mice) with a 3’UTR-trncated Hmga2 cDNA that overexpress Hmga2 mRNA and protein in hematopoietic organs. ∆Hmga2 mice showed proliferative hematopoiesis that mimicked a myeloproliferative neoplasm (MPN)-like phenotype with increased numbers of all lineages of peripheral blood cells, hypercellular bone marrow (BM), splenomegaly with extramedullary erythropoiesis, and erythropoietin-independent erythroid colony formation compared to wild-type mice. ∆Hmga2 BM-derived cells took over most of hematopoiesis in competitive repopulations during serial BM transplants. When we bred mice with circulating PNH cells (Piga- mice) with ∆Hmga2 mice, the lack of GPI-linked proteins did not add an additional clonal advantage to the ∆Hmga2+ cells. In summary, our results showed that the overexpression of a 3’UTR-truncated Hmga2 leads to a proliferative hematopoiesis with clonal advantage, which may explain clonal expansion in PNH or MPN at the level of HSC.
2011-02-06 | GSE24071 | GEO
Project description:Endothelial cells are implicated in delayed thrombus resolution. We use single cell RNA sequencing of CTEPH surgical specimens to assess endothelial cell phenotypes that contribute to delayed thrombus resolution.
2025-07-02 | GSE271435 | GEO