ArticleBlood2005
Distinctive and indispensable roles of PU.1 in maintenance of hematopoietic stem cells and their differentiation.
Article in Blood, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 230 papers.
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Who cites it
230 citing papers in PubMed, 428 citations in OpenAlex.
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- P-selectin delineates conserved functional heterogeneity in early hematopoietic stem cell aging in humans and mice.The EMBO journal · 2026Article
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- Computational Analysis of SPI1 Missense Mutations and ADMET-Guided Molecular Docking of Cinnamic Acid Targeting the PU.1 ETS Domain: Implications for Hematopoietic Dysregulation and Leukemogenesis.International journal of molecular sciences · 2026Article
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- DCAF13 Safeguards Hematopoietic Stem Cells via RRS1-Regulated Ribosome Biogenesis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- The transcription factor EHF promotes the maturation and immunosuppression of conventional dendritic cells.Nature communications · 2026Article
- RORγtScience immunology · 2026Article
- USP7 sustains hematopoietic stem cell homeostasis partially via PU.1 stabilization.International journal of biological sciences · 2026Article
- Chronic Alcohol Consumption Enhances the Differentiation Capacity of Hematopoietic Stem and Progenitor Cells into Osteoclast Precursors.The American journal of pathology · 2026Article
- Distinct roles of Atf3, Zfp711 and Bcl6b in early embryonic hematopoietic and endothelial lineage specification.Development (Cambridge, England) · 2025Article
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- Advances in the characterization of in vitro-generated red blood cells: from biophysical properties to functional applications.Stem cell research & therapy · 2025Review
- Xenophagocytosis blockade enhances interspecies chimerism.bioRxiv : the preprint server for biology · 2025Article
- Coupling CRISPR scanning with targeted chromatin accessibility profiling using a double-stranded DNA deaminase.Nature methods · 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
- One hundred thirty-four germ line PU.1 variants and the agammaglobulinemic patients carrying them.Blood · 2025Article
- A system-level model reveals that transcriptional stochasticity is required for hematopoietic stem cell differentiation.NPJ systems biology and applications · 2024Article
170 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
18 authors at 1 institution in 1 country.
Funding
Abstract
The PU.1 transcription factor is a key regulator of hematopoietic development, but its role at each hematopoietic stage remains unclear. In particular, the expression of PU.1 in hematopoietic stem cells (HSCs) could simply represent "priming" of genes related to downstream myelolymphoid lineages. By using a conditional PU.1 knock-out model, we here show that HSCs express PU.1, and its constitutive expression is necessary for maintenance of the HSC pool in the bone marrow. Bone marrow HSCs disrupted with PU.1 in situ could not maintain hematopoiesis and were outcompeted by normal HSCs. PU.1-deficient HSCs also failed to generate the earliest myeloid and lymphoid progenitors. PU.1 disruption in granulocyte/monocyte-committed progenitors blocked their maturation but not proliferation, resulting in myeloblast colony formation. PU.1 disruption in common lymphoid progenitors, however, did not prevent their B-cell maturation. In vivo disruption of PU.1 in mature B cells by the CD19-Cre locus did not affect B-cell maturation, and PU.1-deficient mature B cells displayed normal proliferation in response to mitogenic signals including the cross-linking of surface immunoglobulin M (IgM). Thus, PU.1 plays indispensable and distinct roles in hematopoietic development through supporting HSC self-renewal as well as commitment and maturation of myeloid and lymphoid lineages.
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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.