ArticleCommunications biology2022
PU.1-c-Jun interaction is crucial for PU.1 function in myeloid development.
Article in Communications biology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 42 citations in OpenAlex.
- Vitamin D Deficiency in Leukemia: Implications for Pathophysiology, Treatment, and Supportive Care.Nutrients · 2026Review
- Quantitative molecular cartography of emergency myelopoiesis reveals conserved modules of hematopoietic activation.Cell stem cell · 2026Article
- Myeloid Mas drives pyruvate kinase M2-mediated Spi1 lactylation to fuel inflammatory senescence in MASLD.Signal transduction and targeted therapy · 2026Article
- Multiomic Profiling Reveals the Regulation of Many Immune-Related Genes by PU.1 in Porcine Alveolar Macrophages.Animals : an open access journal from MDPI · 2026Article
- Discovery of key regulators in classical monocyte phenotypes linked to COVID-19 severity using single-cell multi-omics sequencing.iScience · 2026Article
- Melanoma stem cells drive macrophage reprogramming to a hybrid phenotype, modulating melanoma stemness and compromising NK cell-mediated immunity.Frontiers in immunology · 2026Article
- Neuronal SPI1 suppression enhances axonal regeneration after spinal cord injury through Rassf10 downregulation.Burns & trauma · 2026Article
- Microbial cancer immunotherapy reprograms hematopoiesis to enhance myeloid-driven anti-tumor immunity.Cancer cell · 2025Article
- PU.1/Spi1 exacerbates ischemia-reperfusion induced acute kidney injury via upregulating Gata2 and promoting fibroblast activation.Acta pharmacologica Sinica · 2025Article
- The ETS-family transcription factor PU.1 is a critical regulator of the inhibitory Fcγ receptor IIB expression in humans.Journal of immunology (Baltimore, Md. : 1950) · 2025Article
- Senescence-associated lineage-aberrant plasticity evokes T-cell-mediated tumor control.Nature communications · 2025Article
- Synovial macrophage diversity and activation of M-CSF signaling in post-traumatic osteoarthritis.eLife · 2025Article
- Article
- Integrative multi-omics analysis of IFNγ-induced macrophages and atherosclerotic plaques reveals macrophage-dependent STAT1-driven transcription in atherosclerosis.Frontiers in immunology · 2025Article
- Splicing the Difference: Harnessing the Complexity of the Transcriptome in Hematopoiesis.Experimental hematology · 2024Review
- A Study ofGenes · 2024Article
- YY1 knockout in pro-B cells impairs lineage commitment, enabling unusual hematopoietic lineage plasticity.Genes & development · 2024Article
- The role of lipoprotein‑associated phospholipase A2 in inflammatory response and macrophage infiltration in sepsis and the regulatory mechanisms.Functional & integrative genomics · 2024Article
- Regulation of developmentally controlled enhancer activity by extrinsic signals in normal and malignant cells: AP-1 at the centre.Frontiers in epigenetics and epigenomics · 2024Article
- The Proteomic Landscape of Monocytes in Response to Colorectal Cancer Cells.Journal of proteome research · 2024Article
Corrections and comments
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Authors and funding
14 authors at 6 institutions in 8 countries.
Funding
Abstract
The Ets transcription factor PU.1 is essential for inducing the differentiation of monocytes, macrophages, and B cells in fetal liver and adult bone marrow. PU.1 controls hematopoietic differentiation through physical interactions with other transcription factors, such as C/EBPα and the AP-1 family member c-Jun. We found that PU.1 recruits c-Jun to promoters without the AP-1 binding sites. To address the functional importance of this interaction, we generated PU.1 point mutants that do not bind c-Jun while maintaining normal DNA binding affinity. These mutants lost the ability to transactivate a target reporter that requires a physical PU.1-c-Jun interaction, and did not induce monocyte/macrophage differentiation of PU.1-deficient cells. Knock-in mice carrying these point mutations displayed an almost complete block in hematopoiesis and perinatal lethality. While the PU.1 mutants were expressed in hematopoietic stem and early progenitor cells, myeloid differentiation was severely blocked, leading to an almost complete loss of mature hematopoietic cells. Differentiation into mature macrophages could be restored by expressing PU.1 mutant fused to c-Jun, demonstrating that a physical PU.1-c-Jun interaction is crucial for the transactivation of PU.1 target genes required for myeloid commitment and normal PU.1 function in vivo during macrophage differentiation.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.