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- W4385694257 abstract "PTEN loss in fetal liver hematopoietic stem cells (HSCs) leads to alterations in myeloid, T-, and B-lineage potentials and T-lineage acute lymphoblastic leukemia (T-ALL) development. To explore the mechanism underlying PTEN-regulated hematopoietic lineage choices, we carry out integrated assay for transposase-accessible chromatin using sequencing (ATAC-seq), single-cell RNA-seq, and in vitro culture analyses using in vivo-isolated mouse pre-leukemic HSCs and progenitors. We find that PTEN loss alters chromatin accessibility of key lineage transcription factor (TF) binding sites at the prepro-B stage, corresponding to increased myeloid and T-lineage potentials and reduced B-lineage potential. Importantly, we find that PU.1 is an essential TF downstream of PTEN and that altering PU.1 levels can reprogram the chromatin accessibility landscape and myeloid, T-, and B-lineage potentials in Ptennull prepro-B cells. Our study discovers prepro-B as the key developmental stage underlying PTEN-regulated hematopoietic lineage choices and suggests a critical role of PU.1 in modulating the epigenetic state and lineage plasticity of prepro-B progenitors." @default.
- W4385694257 created "2023-08-10" @default.
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- W4385694257 date "2023-08-01" @default.
- W4385694257 modified "2023-10-16" @default.
- W4385694257 title "PTEN regulates hematopoietic lineage plasticity via PU.1-dependent chromatin accessibility" @default.
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- W4385694257 doi "https://doi.org/10.1016/j.celrep.2023.112967" @default.
- W4385694257 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/37561626" @default.
- W4385694257 hasPublicationYear "2023" @default.
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