ArticleThe EMBO journal1996
Targeted disruption of the PU.1 gene results in multiple hematopoietic abnormalities.
Article in The EMBO journal, 1996. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 423 papers, 1 of them a synthesis that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
423 citing papers in PubMed, 1 synthesis or guideline pooled it, 1,123 citations in OpenAlex.
- Pooled it
- Lineage switch in leukemia and lymphoma: case reports and molecular and cellular mechanisms.Blood neoplasia · 2026Review
- Dynamic metabolic programming of monocyte-derived cells defines immunity in CNS disease.Brain : a journal of neurology · 2026Review
- Review
- Signal-integrated control of immune and reparative programs establishes blood-derived fibrocytes reprogrammable toward induced pluripotency.Biology open · 2026Article
- The Epigenetic Architecture of Classical Hodgkin Lymphoma: Lineage Erasure, Immune Escape, and Therapeutic Reprogramming.Medicina (Kaunas, Lithuania) · 2026Review
- Article
- Macrophages in embryonic development.Nature reviews. Immunology · 2026Review
- MORC3 represses a tandem repeat enhancer to regulate interferon.The EMBO journal · 2026Article
- Review
- PU.1 is a mediator of the reactive stromal response associated with castration-resistant prostate cancer.Communications biology · 2026Article
- Epigenetic profiling of hematopoietic stem cells from male mice identifies KDR and PU.1 as regulators of aging transcriptome and caloric restriction response.Nature communications · 2026Article
- MerTK-triggered TGFβ1 autocrine signal regulates microglial response to neurodegeneration.Nature communications · 2026Article
- Chimeric brain models to study human glial-neuronal and macroglial-microglial interactions.Cell reports · 2026Article
- Cell signaling and transcriptional regulation of osteoclast lineage commitment, differentiation, bone resorption and diseases.Cell discovery · 2026Review
- Microglia across evolution: from conserved origins to functional divergence.Cellular & molecular immunology · 2025Review
- Xenophagocytosis blockade enhances interspecies chimerism.bioRxiv : the preprint server for biology · 2025Article
- Fetal lymphocyte progenitors efficiently generate innate-like B cells but make a more limited contribution to the production of conventional lymphocytes.Experimental hematology · 2025Review
- Article
- Lysine-specific demethylase 1 regulates hematopoietic stem cell expansion and myeloid cell differentiation.Cell death & disease · 2025Article
363 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors at 1 institution in 1 country.
Funding
Abstract
PU.1 is a member of the ets family of transcription factors and is expressed exclusively in cells of the hematopoietic lineage. Mice homozygous for a disruption in the PU.1 DNA binding domain are born alive but die of severe septicemia within 48 h. The analysis of these neonates revealed a lack of mature macrophages, neutrophils, B cells and T cells, although erythrocytes and megakaryocytes were present. The absence of lymphoid commitment and development in null mice was not absolute, since mice maintained on antibiotics began to develop normal appearing T cells 3-5 days after birth. In contrast, mature B cells remained undetectable in these older mice. Within the myeloid lineage, despite a lack of macrophages in the older antibiotic-treated animals, a few cells with the characteristics of neutrophils began to appear by day 3. While the PU.1 protein appears not to be essential for myeloid and lymphoid lineage commitment, it is absolutely required for the normal differentiation of B cells and macrophages.
Indexed as
Identifiers
8896458PMC452309W1483582136What OpenQuestion holds
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.