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Loss of ATF4 leads to functional aging-like attrition of adult hematopoietic stem cells [RNA-seq]

ABSTRACT: Loss of ATF4 leads to functional aging-like attrition of adult hematopoietic stem cells [RNA-seq]

PROVIDER: PRJNA548749 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR16027456_1.fastq.gz	Fastqsanger.gz
	SRR16027456_2.fastq.gz	Fastqsanger.gz
	SRR16027457_1.fastq.gz	Fastqsanger.gz
	SRR16027457_2.fastq.gz	Fastqsanger.gz
	SRR16027458_1.fastq.gz	Fastqsanger.gz

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Loss of ATF4 leads to functional aging-like attrition of adult hematopoietic stem cells

Project description:Loss of ATF4 leads to functional aging-like attrition of adult hematopoietic stem cells

| PRJNA548746 | ENA

Loss of ATF4 leads to functional aging-like attrition of adult hematopoietic stem cells [ChIP-seq]

Project description:Loss of ATF4 leads to functional aging-like attrition of adult hematopoietic stem cells [ChIP-seq]

| PRJNA548750 | ENA

Loss of ATF4 leads to functional aging-like attrition of adult hematopoietic stem cells [RNA-seq]

Project description:We collected significant amount of phenotypic and mechanistic data from a ATF4 knockout mouse model and demonstrated that HSC defects with an aging-like phenotype (expanded pool of phenotypical HSCs, decreased number of functional HSCs, impaired repopulating and self-renewal capacities of HSCs and myeloid bias) occurred in the ATF4 KO mice, suggesting that not only ATF4 indeed represents a pivotal factor for adult HSC function but also we had successfully constructed an ideal and attractive model to study aging and aging-related disease.

2021-12-29 | GSE132682 | GEO

Loss of ATF4 leads to functional aging-like attrition of adult hematopoietic stem cells [ChIP-seq]

Project description:Human acute myeloid leukemia (AML) KG1a cells or mouse BM cells (mouse bone morrow cells were employed for each ChIP assay. The ChIP procedure was performed according to a previously described protocol (Lee et al., 2006; Ying et al., 2017), using anti-ATF4 antibody (Abcam)

2021-12-29 | GSE132681 | GEO

Loss of ATF4 leads to functional aging-like attrition of adult hematopoietic stem cells.

Project description:[Figure: see text].

| S-EPMC8694622 | biostudies-literature

Loss of ATF4 leads to functional aging-like attrition of adult hematopoietic stem cells

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

2021-12-29 | GSE132683 | GEO

Attrition of X chromosome inactivation in aged hematopoietic stem cells

Project description:Attrition of X chromosome inactivation in aged hematopoietic stem cells

| PRJNA703945 | ENA

RNA-seq of muscles from young and aged ATF4 mKO mice and littermate controls

Project description:To investigate the roles of ATF4 in skeletal muscle aging we generated muscle-specific ATF4 knockout (ATF4 mKO) mice. We then performed gene expression profiling analysis using data obtained from RNA-seq of tibialis anterior muscles at 6-months and 22-months of age.

2023-05-02 | GSE212675 | GEO

Hematopoiesis under telomeric attrition at the single-cell resolution

Project description:The molecular mechanisms that drive hematopoietic stem cell (HSC) functional decline under conditions of stress are not completely understood. Here, in light of the recent advances in single-cell technologies, we sought to redefine the transcriptional and epigenetic landscape of mouse and human hematopoietic stem cells (HSCs) under telomeric stress, as that induced by pathogenic germline mutations in telomerase complex genes. These analyses revealed that telomere attrition maintains HSCs in a state of persistent metabolic activation and differentiation towards the megakaryocytic lineage through the cell-intrinsic upregulation of interferon (IFN) signaling response, which directly comprises HSCs’ self-renewal capabilities and eventually leads to their exhaustion. Telomerase reactivation completely restored HSC transcriptional homeostasis at the single-cell level, overcame enhanced megakaryocytic differentiation and significantly ameliorated HSCs’ repopulation capacity in the setting of competitive transplantation, suggesting that HSCs can repristinate their function upon telomere damage resolution. This study challenges the long-standing hypothesis that telomere attrition limits the proliferative potential of HSCs by inducing apoptosis or senescence and suggests that early intervention targeting the IFN axis could prevent bone marrow failure syndromes in patients with pathogenic mutations affecting telomere maintenance.

2021-10-23 | GSE169709 | GEO

ATF4 governs functional expansion of hematopoietic stem cells partially via Angptl3 in the fetal liver microenvironment (array)

Project description:In this study, we demonstrated that deletion of the activating transcription factor 4 (ATF4) resulted in severely impaired HSC expansion in the fetal liver at E12.5 and E15.5. In contrast, generation of the first HSC population in the aorta-gonad-mesonephros region at E11.5 was not significantly affected. Furthermore, the HSC-supporting ability of both endothelial and stromal cells in fetal liver was significantly compromised in the absence of ATF4. Gene profiling using RNA-seq revealed down-regulated expression of a panel of cytokines in ATF4-/- stromal cells, including angiopoietin-like protein 3 (Angptl3) and vascular endothelial growth factor-A (VEGFA). To investigate the molecular pathways of ATF4 in the stromal cells and LSK cells in the fetal liver.

2015-11-20 | E-GEOD-66381 | biostudies-arrayexpress

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