Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

FOS Guards Quiescence and Potency in Human Hematopoietic Stem Cells

ABSTRACT: FOS Guards Quiescence and Potency in Human Hematopoietic Stem Cells

PROVIDER: PRJNA735759 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR14749100_1.fastq.gz	Fastqsanger.gz
	SRR14749100_2.fastq.gz	Fastqsanger.gz
	SRR14749200_1.fastq.gz	Fastqsanger.gz
	SRR14749200_2.fastq.gz	Fastqsanger.gz
	SRR14749300_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 1338

Similar Datasets

FOS Guards Quiescence and Potency in Human Hematopoietic Stem Cells [scRNA-seq]

Project description:Quiescence and limited dividing are critical in preserving potency of hematopoietic stem/progenitor cell (HSPCs) during lifetime, but little is known about how this process is regulated. Here, we show that the mobilized human HSPCs in peripheral blood (PB) are predominantly in a quiescent state, but rapidly exit quiescence and reduce repopulating potency in short-term culture. Through single cell RNA-seq, we identified a panel of regulators highly associated with HSC quiescence exit and cell-cycle entry. These regulators involve different biological processes such as cell-cycle, signaling pathways, metabolisms, etc. Among them, the oncogene, FOS restrains cell-cycle entry and supports repopulating potency in human HSCs through directly binding and regulating genes both for HSC quiescence and potency. Our findings uncover the regulatory program underlying quiescence exit and highlight the critical role of FOS to guard the quiescence and potency in human HSPCs.

2021-06-08 | GSE176272 | GEO

FOS Guards Quiescence and Potency in Human Hematopoietic Stem Cells [RNA-seq]

2021-06-08 | GSE176317 | GEO

FOS Guards Quiescence and Potency in Human Hematopoietic Stem Cells [CUT&Tag]

2021-06-08 | GSE176316 | GEO

FOS Guards Quiescence and Potency in Human Hematopoietic Stem Cells [RNA-seq]

Project description:FOS Guards Quiescence and Potency in Human Hematopoietic Stem Cells [RNA-seq]

| PRJNA735761 | ENA

FOS Guards Quiescence and Potency in Human Hematopoietic Stem Cells [CUT&Tag]

Project description:FOS Guards Quiescence and Potency in Human Hematopoietic Stem Cells [CUT&Tag]

| PRJNA735760 | ENA

FOS Guards Quiescence and Potency in Human Hematopoietic Stem Cells [scRNA-seq]

Project description:FOS Guards Quiescence and Potency in Human Hematopoietic Stem Cells [scRNA-seq]

| PRJNA735710 | ENA

FOS Guards Quiescence and Potency in Human Hematopoietic Stem Cells

Project description:This SuperSeries is composed of the SubSeries listed below.

2021-06-08 | GSE176318 | GEO

p53 Regulates Hematopoietic Stem Cell Quiescence

Project description:The importance of the p53 protein in the cellular response to DNA damage is well known, but its function during steady-state hematopoiesis has not been established. We have defined a critical role of p53 in regulating hematopoietic stem cell quiescence, especially in promoting the enhanced quiescence seen in HSCs that lack the MEF/ELF4 transcription factor. Transcription profiling of HSCs isolated from wild type and p53 null mice identified Gfi-1 and Necdin as p53 target genes and using lentiviral vectors to upregulate or knockdown the expression of these genes, we show their importance in regulating HSC quiescence. Establishing the role of p53 (and its target genes) in controlling the cell cycle entry of HSCs may lead to therapeutic strategies capable of eliminating quiescent cancer (stem) cells.

2008-11-07 | GSE13448 | GEO

FoxM1 is essential for quiescence and maintenance of hematopoietic stem cell

Project description:FoxM1, a mammalian Forkhead Box M1 protein, is known as a typical proliferation-associated transcription factor that regulates of G1/S and G2/M transition in the proliferating cells. However, the in vivo function of FoxM1 in adult stem cells remains unknown. Here, we found that FoxM1 is highly expressed in hematopoietic stem cells (HSCs) and is essential for maintaining quiescence and self-renewal of HSCs in vivo. FoxM1-deficient mice developed leukopenia, thrombocytopenia and neutropenia with an approximately 6-fold decrease in HSC pool size, which is associated with a failure of G0 cell cycle regulation and increased cell cycling in HSCs. FoxM1 absence did not affect lineage commitment of HSCs and progenitors. However, FoxM1 loss significantly reduced the repopulating capacity and self-renewal of long-term HSC in a cell-autonomous manner. Mechanistically, FoxM1 loss markedly down-regulates the expression of orphan nuclear receptor Nurr1, known to regulate HSC quiescence. We found that FoxM1 directly bound the promoter region of Nurr1 and induced transcriptional activity of Nurr1 promoter in vitro, and forced expression of Nurr1 rescued FoxM1-deletion-induced G0 loss of HSC-enriched population in vitro. Thus, our studies show a previously unrecognized role of FoxM1 as a critical regulator of HSC quiescence and self-renewal by controlling Nurr1-mediated pathways. The Hematopoietic Stem Cells (HSCs) were sorted from FoxM1[fl/fl] and Tie2-Cre FoxM1[fl/fl] mice, then amplified with Ovation Pico WTA System V2 before microarray analysis. There are 3 samples from FoxM1[fl/fl]mice and 3 samples from Tie2-Cre FoxM1[fl/fl] mice.

2015-06-15 | E-GEOD-62360 | biostudies-arrayexpress

Retinoid X receptor promotes hematopoietic stem cell fitness and quiescence and preserves hematopoietic homesotasis [Bulk]

Project description:Hematopoietic stem cells (HSCs) balance self-renewal and differentiation to maintain hematopoietic fitness throughout life. In steady-state conditions, HSC exhaustion is prevented by the maintenance of most HSCs in a quiescent state, with cells entering the cell cycle only occasionally. HSC quiescence is regulated by retinoid and fatty-acid ligands of transcriptional factors of the nuclear retinoid X receptor (RXR) family. Here, we show that dual deficiency for hematopoietic RXRa and RXRb induces HSC exhaustion, myeloid cell/megakaryocyte differentiation, and myeloproliferative-like disease. RXRa and RXRb maintain HSC quiescence, survival, and chromatin compaction; moreover, transcriptome changes in RXRa;RXRb-deficient HSCs include premature acquisition of an aging-like HSC signature, MYC pathway upregulation, and RNA intron retention. Fitness loss and associated RNA transcriptome and splicing alterations in RXRa;RXRb-deficient HSCs are prevented by Myc haploinsufficiency. Our study reveals the critical importance of RXRs for the maintenance of HSC fitness and their protection from premature aging.

2022-11-11 | GSE191161 | 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