ArticleBlood2011
Two distinct auto-regulatory loops operate at the PU.1 locus in B cells and myeloid cells.
Article in Blood, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 78 papers.
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.
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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
78 citing papers in PubMed, 132 citations in OpenAlex.
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- Boolean logic links chromatin accessibility states to gene expression variability across cell types.Nucleic acids research · 2026Article
- The epigenetic circle: feedback loops in the maintenance of cellular memory.Epigenetics & chromatin · 2025Review
- Chromatin structure and 3D architecture define the differential functions of PU.1 regulatory elements in blood cell lineages.Epigenetics & chromatin · 2024Article
- Chromatin priming elements direct tissue-specific gene activity before hematopoietic specification.Life science alliance · 2024Article
- From Genotype to Phenotype: How Enhancers Control Gene Expression and Cell Identity in Hematopoiesis.HemaSphere · 2023Review
- Carm1-arginine methylation of the transcription factor C/EBPα regulates transdifferentiation velocity.eLife · 2023Article
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- A genome-wide relay of signalling-responsive enhancers drives hematopoietic specification.Nature communications · 2023Article
- Unveiling the complexity of transcription factor networks in hematopoietic stem cells: implications for cell therapy and hematological malignancies.Frontiers in oncology · 2023Review
- Article
- Combined Approach to Leukemic Differentiation Using Transcription Factor PU.1-Enhancing Agents.International journal of molecular sciences · 2022Article
- Blood stem cell PU.1 upregulation is a consequence of differentiation without fast autoregulation.The Journal of experimental medicine · 2022Article
- Data-driven modeling predicts gene regulatory network dynamics during the differentiation of multipotential hematopoietic progenitors.PLoS computational biology · 2022Article
- Genomic and epigenomic adaptation in SP-R210 (Myo18A) isoform-deficient macrophages.Immunobiology · 2021Article
- Logic and lineage impacts on functional transcription factor deployment for T-cell fate commitment.Biophysical journal · 2021Review
- Modest changes in Spi1 dosage reveal the potential for altered microglial function as seen in Alzheimer's disease.Scientific reports · 2021Article
- A network-based computational framework to predict and differentiate functions for gene isoforms using exon-level expression data.Methods (San Diego, Calif.) · 2021Article
- Multi-scale Dynamical Modeling of T Cell Development from an Early Thymic Progenitor State to Lineage Commitment.Cell reports · 2021Article
18 more citing papers are in PubMed but not listed here.
Corrections and comments
- Erratum issued
Authors and funding
17 authors at 5 institutions in 4 countries.
Funding
Abstract
The transcription factor PU.1 occupies a central role in controlling myeloid and early B-cell development, and its correct lineage-specific expression is critical for the differentiation choice of hematopoietic progenitors. However, little is known of how this tissue-specific pattern is established. We previously identified an upstream regulatory cis element whose targeted deletion in mice decreases PU.1 expression and causes leukemia. We show here that the upstream regulatory cis element alone is insufficient to confer physiologic PU.1 expression in mice but requires the cooperation with other, previously unidentified elements. Using a combination of transgenic studies, global chromatin assays, and detailed molecular analyses we present evidence that PU.1 is regulated by a novel mechanism involving cross talk between different cis elements together with lineage-restricted autoregulation. In this model, PU.1 regulates its expression in B cells and macrophages by differentially associating with cell type-specific transcription factors at one of its cis-regulatory elements to establish differential activity patterns at other elements.
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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.