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ONTOGENY SHAPES THE ABILITY OF ETV6-RUNX1 TO ENHANCE HEMATOPOIETIC STEM CELL SELF-RENEWAL AND DISRUPT EARLY LYMPHOPOIESIS

ABSTRACT: ONTOGENY SHAPES THE ABILITY OF ETV6-RUNX1 TO ENHANCE HEMATOPOIETIC STEM CELL SELF-RENEWAL AND DISRUPT EARLY LYMPHOPOIESIS

PROVIDER: PRJNA998835 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR25434159_1.fastq.gz	Fastqsanger.gz
	SRR25434159_2.fastq.gz	Fastqsanger.gz
	SRR25434160_1.fastq.gz	Fastqsanger.gz
	SRR25434160_2.fastq.gz	Fastqsanger.gz
	SRR25434161_1.fastq.gz	Fastqsanger.gz

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ONTOGENY SHAPES THE ABILITY OF ETV6-RUNX1 TO ENHANCE HEMATOPOIETIC STEM CELL SELF-RENEWAL AND DISRUPT EARLY LYMPHOPOIESIS [in vitro]

Project description:ONTOGENY SHAPES THE ABILITY OF ETV6-RUNX1 TO ENHANCE HEMATOPOIETIC STEM CELL SELF-RENEWAL AND DISRUPT EARLY LYMPHOPOIESIS [in vitro]

| PRJNA998850 | ENA

ONTOGENY SHAPES THE ABILITY OF ETV6-RUNX1 TO ENHANCE HEMATOPOIETIC STEM CELL SELF-RENEWAL AND DISRUPT EARLY LYMPHOPOIESIS [in vivo]

Project description:ONTOGENY SHAPES THE ABILITY OF ETV6-RUNX1 TO ENHANCE HEMATOPOIETIC STEM CELL SELF-RENEWAL AND DISRUPT EARLY LYMPHOPOIESIS [in vivo]

| PRJNA998849 | ENA

Ontogeny shapes the ability of ETV6::RUNX1 to enhance hematopoietic stem cell self-renewal and disrupt early lymphopoiesis.

Project description: Not available

| S-EPMC10844086 | biostudies-literature

ONTOGENY SHAPES THE ABILITY OF ETV6-RUNX1 TO ENHANCE HEMATOPOIETIC STEM CELL SELF-RENEWAL AND DISRUPT EARLY LYMPHOPOIESIS [in vitro]

Project description:The ETV6-RUNX1 (E/R) translocation, found in approximately 30% of pediatric B-cell acute lymphoblastic leukemia (ALL) cases, originates prenatally. Although hematopoietic stem cells (HSCs) have been proposed as the cell of origin for E/R-ALL, definitive evidence for this has been lacking. Here, we develop an E/R-inducible transgenic mouse model and observe that E/R rapidly expands the pool of phenotypic HSCs and block early B cell development. By leveraging the reversibility of the model, we demonstrate functional rather than merely phenotypic HSC expansion. At a molecular level, E/R activates immune checkpoint pathways, which is more pronounced in fetal cells. Comparison of fetal and adult HSCs reveals that although E/R disrupts HSC differentiation in both, fetal cells have a competitive advantage, especially in a setting of viral mimicry. These findings provide new insights into the nature of preleukemic clones associated with E/R and suggest potential benefits of immune checkpoint inhibition for their eradication.

2024-01-08 | GSE239342 | GEO

ONTOGENY SHAPES THE ABILITY OF ETV6-RUNX1 TO ENHANCE HEMATOPOIETIC STEM CELL SELF-RENEWAL AND DISRUPT EARLY LYMPHOPOIESIS [in vivo]

2024-01-08 | GSE239340 | GEO

ONTOGENY SHAPES THE ABILITY OF ETV6-RUNX1 TO ENHANCE HEMATOPOIETIC STEM CELL SELF-RENEWAL AND DISRUPT EARLY LYMPHOPOIESIS

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

2024-01-08 | GSE239344 | GEO

Identification of ETV6 bound protein by affinity purification of ETV6-HA fusion protein in REH cells

Project description:To determine the protein partners of ETV6, we expressed ETV6 and HA-tagged ETV6 in Reh pre-B leukemic cells. Anti-HA magnetic beads were used for affinity purification of ETV6-HA (and ETV6 control) from the nuclear and cytoplasmic fraction. Following purification on-beads digest and LC-MS/MS experiments were performed at the Proteomics platform of the CHU de Quebec Research Center, Quebec, Canada.

2022-01-26 | PXD031001 | Pride

A germline ETV6 mutation disrupts hematopoiesis via de novo creation of a nuclear export signal

Project description:Germline mutations in the transcriptional regulator ETV6 are a root cause of familial inherited thrombocytopenia and predispose carriers to myelodysplastic syndromes and acute leukemias. Here, we report that the ETV6 P214L mutation creates an XPO1-dependent nuclear export signal to cause protein mislocalization. Strategies to disrupt XPO1 nuclear export activity fully restore ETV6 P214L protein nuclear localization and transcription regulation activity, establishing XPO1-dependent mislocalization as a critical mechanism underscoring ETV6 P214L dysfunction. Mechanistic insight inspired the design of ‘humanized’ ETV6 mice in which the germline P214L mutation is sufficient to elicit severe defects in thrombopoiesis and hematopoietic stem cell maintenance and survival in animals. These studies define a unique mechanism by which the ETV6 P214L mutation exerts a dominant negative effect on protein function and reveal critical mutation-dependent disruptions to hematopoiesis that underlie disease phenotypes.

2025-04-23 | GSE287784 | GEO

A germline ETV6 mutation disrupts hematopoiesis via de novo creation of a nuclear export signal

2025-04-11 | GSE288171 | GEO

ETV6-NCOA2 expression profile in T/M mixed-phenotype acute leukemia [ETV6-NCOA2 human]

Project description:Exparession profiling of ETV6-NCOA2 at different stages of disease dEmpty vectorelopment: CD34 cord blood cells transduced with ETV6-NCOA2-GFP or with empty vector-GFP, CD34 cord blood cells transduced with ETV6-NCOA2-NGFR or ETV6-NCOA2-NGFR + NOTCH1-L1601PdP-GFP and transplanted in NSGS mice, and ETV6-NCOA2 patient derived xenografts.

2022-05-16 | GSE161702 | GEO

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