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Leukemia-mutated proteins PHF6 and PHIP form a chromatin complex that represses acute myeloid leukemia stemness

ABSTRACT: Leukemia-mutated proteins PHF6 and PHIP form a chromatin complex that represses acute myeloid leukemia stemness

PROVIDER: PRJNA1255662 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR31295663_1.fastq.gz	Fastqsanger.gz
	SRR31295663_2.fastq.gz	Fastqsanger.gz
	SRR31295664_1.fastq.gz	Fastqsanger.gz
	SRR31295664_2.fastq.gz	Fastqsanger.gz
	SRR31295665_1.fastq.gz	Fastqsanger.gz

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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

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

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Transcriptomic changes in THP1 human AML cell line on PHF6 knockout, PHF6R274Q mutation, PHIP knockout, and double knockout of PHF6 and PHIP compared to wildtype cells

Project description:PHF6 is a transcriptional regulator mutated in 3-5% of acute myeloid leukemia. To understand the effect of loss and clinical mutation of PHF6 on the transcriptome of myeloid cells, we generated multiple wildtype and PHF6 knockout clones, as well as clones expressing the most common clinical mutant of the protein-PHF6R274Q. We observed that both single and double knockouts and mutation of PHF6 shifted the cells towards stemness and away from differentiation. Additionally we identified PHIP as a possible functional partner for PHF6. To investigate their common biological function, we generated multiple single knockout clones of PHIP as well as double knockout clones of PHIP and PHF6, and observed that, similar to single knockout of PHF6, PHIP knockout and double knockout also shifted cells towards stemness and away from differentiation. Collectively, our experiments show that PHF6 and PHIP, separately identified as being mutated in AML, exert similar downstream effects on the AML transcriptome.

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Transcriptomic changes in PHF6 knockout THP1 human AML cell line on rescue with PHF6 wildtype (with and without PHIP) or rescue with PHF6R274Q mutant

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Leukemia-mutated proteins PHF6 and PHIP form a chromatin complex that represses acute myeloid leukemia stemness.

Project description: Not available

| S-EPMC11642813 | biostudies-literature

Leukemia mutated proteins PHF6 and PHIP form a chromatin complex that represses acute myeloid leukemia stemness.

Project description: Not available

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PHIP occupancy in THP1 human AML cell line

2024-11-15 | GSE281629 | 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

Leukemia-mutated proteins PHF6 and PHIP form a chromatin complex that represses acute myeloid leukemia stemness

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

2025-04-26 | GSE295715 | GEO

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

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