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ABSTRACT: Nuclear Vav3 is required for canonical PRC1 activity in B-cell acute lymphoblastic leukemia

PROVIDER: PRJNA675836 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR13018626_1.fastq.gz	Fastqsanger.gz
	SRR13018626_2.fastq.gz	Fastqsanger.gz
	SRR13018627_1.fastq.gz	Fastqsanger.gz
	SRR13018627_2.fastq.gz	Fastqsanger.gz
	SRR13018628_1.fastq.gz	Fastqsanger.gz

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Nuclear Vav3 is required for canonical PRC1 activity in B-cell lymphoblastic leukemogenesis

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Nuclear Vav3 is required for canonical PRC1 activity in B-cell lymphoblastic leukemogenesis (RNA-Seq)

Project description:Acute B-cell lymphoblastic leukemia (B-ALL) represents a multiclonal evolution of B-cell progenitors endowed with both tumor-initiating and propagating properties. We have previously shown that the concurrent overexpression and activation of both the Rac guanine nucleotide exchange factor (RacGEF) Vav3 and Rac GTPases is required for BCR-ABL-mediated leukemogenesis. Here, we show that upon BCR-ABL expression, Vav3 expression becomes predominantly nuclear. In this location, Vav2 interacts with BCR-ABL, Rac, and the canonical polycomb repression complex proteins Bmi1, Ring1b and Ezh2. The GEF activity of Vav3 is required for B-cell proliferation and Bmi1-dependent B-cell progenitor self-renewal, nuclear Rac activation, protein interaction with Bmi1, H2A(K119) mono-ubiquitination (H2AK119Ub), and repression of downstream target loci. Vav3 deficiency results in de-repression and repression of loci encoding negative regulators of cell proliferation and oncogenic transcriptional factors, respectively. Mechanistically, we show that Vav3 prevents the Phlpp2-sensitive and Akt (S473)-dependent phosphorylation of Bmi1 on the regulatory residue S314 that, in turn, promotes the transcriptional factor reprogramming of leukemic B-cell progenitors. These results highlight the importance of non-canonical nuclear Rho GTPase signaling in leukemogenesis.

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