ArticleThe EMBO journal1998
PU.1 regulates both cytokine-dependent proliferation and differentiation of granulocyte/macrophage progenitors.
Article in The EMBO journal, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 100 papers.
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Who cites it
100 citing papers in PubMed, 295 citations in OpenAlex.
- Review
- Multitissue, multi-time point transcriptomic atlas of aging in mice and rats.Science advances · 2026Article
- Balancing inflammatory signaling in hematopoiesis: roles of MIRC11 and miR-146a.Frontiers in immunology · 2026Article
- "Double-duty" dendritic cells in Xenopus laevis: Early vertebrate splenic APCs resemble conventional dendritic cells and limit native antigen presentation to B cells during a humoral response.Molecular immunology · 2026Article
- A multi-omic atlas of human autonomic and sensory ganglia implicates cell types in peripheral neuropathies.bioRxiv : the preprint server for biology · 2025Article
- Macrophages and fibroblasts as regulators of the immune response in pancreatic cancer.Nature immunology · 2025Review
- Redistribution of PU.1 partner transcription factor RUNX1 binding secures cell survival during leukemogenesis.The EMBO journal · 2024Article
- SPI1Journal for immunotherapy of cancer · 2024Article
- Spi1 regulates the microglial/macrophage inflammatory response via the PI3K/AKT/mTOR signaling pathway after intracerebral hemorrhage.Neural regeneration research · 2024Article
- TLR7 activation at epithelial barriers promotes emergency myelopoiesis and lung antiviral immunity.eLife · 2023Article
- MicroRNAs-mediated regulation pathways in rheumatic diseases.Inflammopharmacology · 2023Review
- PU.1 is required to restrain myelopoiesis during chronic inflammatory stress.Frontiers in cell and developmental biology · 2023Article
- Monocyte Subsets With High Osteoclastogenic Potential and Their Epigenetic Regulation Orchestrated by IRF8.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2021Article
- PU.1 Mimic Synthetic Peptides Selectively Bind with GATA-1 and Allow c-Jun PU.1 Binding to Enhance Myelopoiesis.International journal of nanomedicine · 2021Article
- Article
- Microglia in the developing retina.Neural development · 2019Review
- The transcription factor PU.1 mediates enhancer-promoter looping that is required for IL-1β eRNA and mRNA transcription in mouse melanoma and macrophage cell lines.The Journal of biological chemistry · 2019Article
- Regulation of Osteoclast Differentiation and Skeletal Maintenance by Histone Deacetylases.Molecules (Basel, Switzerland) · 2019Review
- Decreased Expression of Negative Immune Checkpoint VISTA by CD4+ T Cells Facilitates T Helper 1, T Helper 17, and T Follicular Helper Lineage Differentiation in GCA.Frontiers in immunology · 2019Article
- Environmental sensing by mature B cells is controlled by the transcription factors PU.1 and SpiB.Nature communications · 2017Article
40 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
PU.1 is a unique regulatory protein required for the generation of both the innate and the adaptive immune system. It functions exclusively in a cell-intrinsic manner to control the development of granulocytes, macrophages, and B and T lymphocytes. We demonstrate that mutation of the PU.1 gene causes a severe reduction in myeloid (granulocyte/macrophage) progenitors. PU.1 -/- myeloid progenitors can proliferate in vitro in response to the multilineage cytokines interleukin-3 (IL-3), IL-6 and stem cell factor but are unresponsive to the myeloid-specific cytokines granulocyte-macrophage colony-stimulating factor (GM-CSF), G-CSF and M-CSF. The failure of PU.1 -/- progenitors to respond to G-CSF is bypassed by transient signaling with IL-3. In the presence of IL-3 and G-CSF, PU.1 -/- progenitors can differentiate into granulocytic precursors containing myeloperoxidase-positive granules. Thus PU.1 is not essential for specification of granulocytic precursors, but is required for their further differentiation. The failure of PU.1 -/- progenitors to respond to M-CSF is due to lack of c-fms gene transcription. Transduction of c-fms into PU.1 -/- myeloid progenitors bypasses the block to M-CSF-dependent proliferation but does not induce detectable macrophage differentiation. Therefore, PU. 1 appears to be essential for specification of monocytic precursors. Importantly, retroviral transduction of PU.1 into mutant progenitors restores responsiveness to myeloid-specific cytokines and development of mature granulocytes and macrophages. Thus PU.1 controls myelopoiesis by regulating both proliferation and differentiation pathways.
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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.