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

GSE281626 Homo sapiens Genome binding/occupancy profiling by high throughput sequencing 9 samples Submitted 2024/11/15 Platform GPL18573
Summary
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.
Published in
Leukemia mutated proteins PHF6 and PHIP form a chromatin complex that represses acute myeloid leukemia stemness
Pawar AS, Somers P, Alex A et al. · Genes & development 2025 · PMID 40721297 · doi:10.1101/gad.352602.125
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Also filed as BioProject PRJNA1184837 and SRA study SRP544550. Searching any of these in the dataset finder brings you back here.

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