Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Single cell RNA sequencing of HSC and MPP in DNA damage tolerant deficient mutants

ABSTRACT: Single cell RNA sequencing of HSC and MPP in DNA damage tolerant deficient mutants

PROVIDER: PRJNA506282 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR8223370_1.fastq.gz	Fastqsanger.gz
	SRR8223370_2.fastq.gz	Fastqsanger.gz
	SRR8223380_1.fastq.gz	Fastqsanger.gz
	SRR8223380_2.fastq.gz	Fastqsanger.gz
	SRR8223390_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 96

Similar Datasets

CD71+ HSC/MPP

Project description:CD71+ HSC/MPP

| PRJNA789602 | ENA

Single cell RNA sequencing of HSC and MPP in DNA damage tolerant deficient mutants

Project description:We performed scRNA-seq according to the CEL-seq2 protocol in order to define transcriptome changes in mouse hematopoietic stem cell containing LSKs in different mutants with defects in DNA damage tolerances.

2021-01-20 | GSE122784 | GEO

Transcription profiling of Pairwise comparisons of purified mouse LT-HSC, ST-HSC and MPP

Project description:Pairwise comparisons of purified mouse LT-HSC, ST-HSC and MPP.

2005-09-09 | E-SMDB-3457 | biostudies-arrayexpress

CD71+ HSC/MPP

Project description:We describe the unique enrichment of erythroid-megakaryocyte primed CD71+ phenotypic HSC/MPPs in steady-state PB.

2021-12-17 | GSE191084 | GEO

Comparative analysis of 1-methyl-4-phenylpyridinium (MPP+) and manganese induced neurotoxic effects on DNA methylation in dopaminergic neurons

Project description:Idiopathic Parkinson’s disease (iPD) and manganese-induced atypical Parkinsonism are characterized by movement disorder and nigrostriatal pathology. Although clinical features, brain region involved and responsiveness to L-DOPA differentiate both, the differences at the neuronal level are largely unknown. We investigated the morphological, physiological and molecular differences in dopaminergic neurons exposed to the PD toxin 1-methyl-4-phenylpyridinium ion (MPP+) and manganese (Mn). While Mn was neurotoxic at lower dose, MPP+ toxicity entailed oxidative damage, mitochondria dysfunction and glycolytic shift. Morphological analysis highlighted mitochondrial damage, while morphometric analysis indicated loss of neuronal processes in the MPP+ model and not in the Mn model. Elecrophysiological analysis demonstrated lower number of spikes and firing frequency in MPP+ treated cells, while it was unchanged in the Mn model. High throughput transcriptomic analysis revealed upregulation of 694 and 603 genes and down-regulation of 428 and 255 genes in the MPP+ and Mn models respectively. Many differentially expressed genes were unique to either models and contributed to neuroinflammation, metabolic and mitochondrial function, apoptosis and nuclear function, synaptic plasticity, neurotransmission and cytoskeletal architecture. Analysis of the JAK-STAT pathway with implications for neuritogenesis, neuronal proliferation and nuclear function revealed contrasting profile between Mn and MPP+ models. Genome-wide DNA methylation profile revealed significant differences between both models and substantiated the epigenetic basis of the difference in the JAK-STAT pathway. We conclude that iPD and atypical Parkinsonism represent a divergent neurotoxicological manifestation at the dopaminergic neuronal level with implications for pathobiology and to evolve novel therapeutics

2017-10-04 | GSE92691 | GEO

Inhibition of mitochondrial transcription by the neurotoxin MPP+

Project description:The neurotoxin MPP+ triggers cell death of dopamine neurons and induces Parkinson’s disease symptoms in mice and men, but the immediate transcriptional response to this neurotoxin has not been studied. We therefore treated human SH-SY5Y cells with a low dose (0.1 mM) of MPP+ and measured the effect on nascent transcription by precision run-on sequencing (PRO-seq). We found that transcription of the mitochondrial genome was significantly reduced already after 30 min, whereas nuclear gene transcription was unaffected. Inhibition of respiratory complex I by MPP+ led to reduced ATP production, that may explain the diminished activity of mitochondrial RNA polymerase. Our results show that MPP+ has a direct effect on mitochondrial function and transcription, and that other gene expression or epigenetic changes induced by this neurotoxin are secondary effects that reflect a cellular adaptation program.

2023-06-01 | GSE214243 | GEO

RNA-seq analysis of helios deficient hematopoietic stem and progenitor cells.

Project description:Here we addressed the mRNA transcriptome of Long-Term Hematopoietic Stem Cells (LT-HSC) and Multipotent Progenitor (MPP) -3 and -4 purified from WT and Helios KO mice. By analyzing the differentially expressed genes among WT and KO condition we found that Helios deletion affects transcription mostly in the LT-HSC compartment and favor a megakaryocyte mRNA lineage priming at the expense of the lymphoid one.

2021-08-13 | GSE149244 | GEO

Integrated insight into the molecular mechanisms of selenium modulates MPP+ induced cytotoxicity in Parkinson’s disease model

Project description:Parkinson’s disease (PD) is a common neurodegenerative disease, which associated with oxidative stress. Due to the antioxidant function of Selenium (Se), it may have a neuroprotective function in PD. Nevertheless, the Se involved and its role in the protective function is still unclear. 1-methyl-4-phenylpyridinium (MPP+), which inhibits mitochondrial respiration, is usually used to produce a reliable PD cellular model. In this study, we discovered that Se could modulate cytotoxicity in MPP+ induced PD model and used genome wide high throughput sequencing to capture the gene expression profiles of MPP+ treatment PC12 cells with or without Se. We identified 351 differentially expressed mRNAs (DEGs) and 14 differentially expressed long non-coding RNAs (DELs) in MPP+ group vs. normal control group, 244 DEGs and 27 DELs in Se + MPP+ group vs. MPP+ group. Functional annotation analysis of DEGs and DELs cis-target genes revealed that they were enriched in reactive oxygen species (ROS) metabolic process and mitochondrial control of apoptosis. Our data suggests that DEGs, Txnrd1, siglec1 and Klf2, and the DEL AABR07044454.1 cis-acting on target gene Cdkn1a, may act a protective function in PD model. For the first time, our study systematically demonstrated that mRNAs and lncRNAs induced by Se involved in neuroprotection in PD and provided new insight into how Se modulates cytotoxicity in MPP+ induced PD model.

2024-10-27 | GSE186702 | GEO

Transcriptome of subsets of human haematopoietic stem cells from non-mobilised peripheral blood of healthy donors and CD71+ HSC/MPP

Project description:Transcriptome of subsets of human haematopoietic stem cells from non-mobilised peripheral blood of healthy donors and CD71+ HSC/MPP

| PRJNA789599 | ENA

RNAseq analysis of murine ITPKB deficient versus wild type LT-HSC

Project description:Tight regulation of hematopoietic stem cell (HSC) homeostasis is essential for life-long hematopoiesis, for preventing blood cancers and for averting bone marrow failure. The underlying mechanisms are incompletely understood. Here, we identify production of inositol-tetrakisphosphate (IP4) by inositoltrisphosphate 3-kinase B (ItpkB) as essential for HSC quiescence and function. Young ItpkB-/- mice accumulated phenotypic HSC and showed extramedullary hematopoiesis. ItpkB-/- HSC were less quiescent and proliferated more than wildtype controls. They downregulated quiescence and stemness associated mRNAs, but upregulated activation, oxidative metabolism, protein synthesis and lineage associated transcripts. Although they showed no significant homing defects, ItpkB-/- HSC had a severely reduced competitive long-term repopulating potential. Aging ItpkB-/- mice lost hematopoietic stem and progenitor cells and died with severe anemia. Wildtype HSC normally repopulated ItpkB-/- hosts, incidating a HSC-intrinsic ItpkB requirement. ItpkB-/- HSC had reduced cobblestone-area forming cell activity in vitro and showed increased stem-cell-factor activation of the phosphoinositide 3-kinase (PI3K) effector Akt, reversed by exogenous provision of the known PI3K/Akt antagonist IP4. They also showed transcriptome changes consistent with hyperactive Akt/mTOR signaling. Thus, we propose that ItpkB ensures HSC quiescence by limiting cytokine-induced PI3K signaling in HSC.

2015-03-31 | GSE56613 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data