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Mus musculus

ABSTRACT: PHF6 regulates B-cell identity in acute lymphoblastic leukemia [ChIP-Seq]

PROVIDER: PRJNA301714 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR2932266.fastq.gz	Fastqsanger.gz
	SRR2932267.fastq.gz	Fastqsanger.gz
	SRR2932268.fastq.gz	Fastqsanger.gz
	SRR2932269.fastq.gz	Fastqsanger.gz

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Mus musculus

Project description:PHF6 regulates B-cell identity in acute lymphoblastic leukemia

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Project description:PHF6 regulates B-cell identity in acute lymphoblastic leukemia [ATAC-Seq]

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Project description:PHF6 regulates B-cell identity in acute lymphoblastic leukemia [RNA-Seq]

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PHF6 regulates B-cell identity in acute lymphoblastic leukemia

Project description:PHF6 regulates B-cell identity in acute lymphoblastic leukemia

| PRJNA310410 | ENA

RNA sequencing of isogenic Phf6 wild type and Phf6 knockout mouse T-ALL cells

Project description:Loss-of-function mutations Phf6 occur frequently in both adult and pediatric T-cell Acute Lymphoblastic Leukemia (T-ALL). Although Phf6 is widely expressed, little is known about its proposed function as epigenetic regulator and tumor suppressor. To address the role of Phf6 in the leukemia development, here we analyze by RNAseq the gene expression profiles of isogenic Phf6 wild type and Phf6 knockout leukemia cells transformed by overexpression of an oncogenic mutant form of the NOTCH1 receptor.

2019-07-31 | GSE117165 | GEO

Chromatin accessibility changes caused by PHF6 knockout in THP1 human AML cell line

Project description:PHF6 is a transcriptional regulator mutated in 3-5% of acute myeloid leukemia. To understand how PHF6 and its functional partner PHIP interact with each other on chromatin, we performed ChIP-Seq for PHF6 (in the presence and absence of PHIP), and for PHIP. We observd that PHF6 and PHIP peaks overlap on chromatin, and PHF6 requires PHIP for its chromatin occupancy. ATAC-Seq and H3K27ac ChIP-Seq showed that PHF6 and PHIP occupy open and active regions of the genome.

2024-11-15 | GSE281626 | GEO

PHIP occupancy in THP1 human AML cell line

Project description:PHF6 is a transcriptional regulator mutated in 3-5% of acute myeloid leukemia. To understand how PHF6 and its functional partner PHIP interact with each other on chromatin, we performed ChIP-Seq for PHF6 (in the presence and absence of PHIP), for PHF6R274Q mutant, and for PHIP. We observd that PHF6 and PHIP peaks overlap on chromatin, and PHF6 requires PHIP for its chromatin occupancy. ATAC-Seq and H3K27ac ChIP-Seq showed that PHF6 and PHIP occupy open and active regions of the genome.

2024-11-15 | GSE281629 | GEO

PHF6 occupancy in THP1 human AML cell line in wildtype, PHF6R274Q mutant, and PHIP knockout cells

Project description:PHF6 is a transcriptional regulator mutated in 3-5% of acute myeloid leukemia. To understand how PHF6 and its functional partner PHIP interact with each other on chromatin, we performed ChIP-Seq for PHF6 (in the presence and absence of PHIP), for PHF6R274Q mutant, and for PHIP. We observd that PHF6 and PHIP peaks overlap on chromatin, and PHF6 requires PHIP for its chromatin occupancy. ATAC-Seq and H3K27ac ChIP-Seq showed that PHF6 and PHIP occupy open and active regions of the genome.

2024-11-15 | GSE281628 | GEO

Changes in H3K27 acetylation in THP1 human AML cell line on PHF6 knockout, PHF6R274Q mutation, PHIP knockout, and double knockout of PHF6 and PHIP compared to wildtype clones

Project description:PHF6 is a transcriptional regulator mutated in 3-5% of acute myeloid leukemia. To understand how PHF6 and its functional partner PHIP interact with each other on chromatin, we performed ChIP-Seq for PHF6 (in the presence and absence of PHIP), for PHF6R274Q mutant, and for PHIP. We observd that PHF6 and PHIP peaks overlap on chromatin, and PHF6 requires PHIP for its chromatin occupancy. ATAC-Seq and H3K27ac ChIP-Seq showed that PHF6 and PHIP occupy open and active regions of the genome.

2024-11-15 | GSE281627 | GEO

Genome-wide chromatin accessibility profiling of LT-HSCs isolated from WT and Phf6-deficient mice

Project description:The plant homeodomain 6 gene (PHF6) is frequently mutated in human T-cell acute lymphoblastic leukemia (T-ALL); however, its specific functional role in leukemia development remains to be established. Here, we show that loss of PHF6 is an early mutational event in leukemia transformation. Mechanistically, genetic inactivation of Phf6 in the hematopoietic system enhances hematopoietic stem cell (HSC) long-term self-renewal and hematopoietic recovery after chemotherapy by rendering Phf6 knockout HSCs more quiescent and less prone to stress-induced activation. Consistent with a leukemia-initiating tumor suppressor role, inactivation of Phf6 in hematopoietic progenitors lowers the threshold for the development of NOTCH1-induced T-ALL. Moreover, loss of Phf6 in leukemia lymphoblasts activates a leukemia stem cell transcriptional program and drives enhanced T-ALL leukemia-initiating cell activity. These results implicate Phf6 in the control of HSC homeostasis and long-term self-renewal and support a role for PHF6 loss as a driver of leukemia-initiating cell activity in T-ALL.

2021-06-23 | GSE178739 | GEO

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