ReviewFrontiers in immunology2019
Mechanisms of Action of Hematopoietic Transcription Factor PU.1 in Initiation of T-Cell Development.
Review in Frontiers in immunology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 65 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
65 citing papers in PubMed, 104 citations in OpenAlex.
- Trial
- Lamin B1 safeguards the B cell genome and shapes lymphoma outcome.HemaSphere · 2026Article
- Integrated bulk RNA-seq and scRNA-seq identification of a novel "PET-Translational cancer research · 2026Article
- T cell development from expanded hematopoietic progenitors reveals initiation control byScience immunology · 2026Article
- RORγtScience immunology · 2026Article
- Upregulation of CD90 correlates with T lineage commitment at the DN2a stage of T cell development.Frontiers in immunology · 2026Article
- PervasivebioRxiv : the preprint server for biology · 2025Article
- Article
- Novel molecular mechanisms of FLT3 deregulation: from the acute myeloid leukemia experience to therapeutic insights in acute lymphoblastic leukemia.Molecular cancer · 2025Review
- Global human myeloid replacement with peripheral progenitors induces interferonopathy and neurodegeneration.Research square · 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
- Analysis of chromatin accessibility associated with azacitidine response in higher-risk myelodysplastic neoplasms.iScience · 2025Article
- Article
- SPI1 upregulated LILRB2 to enhance the immunosuppressive phenotype of LPS-tolerant macrophages by inhibiting TLR8-mediated MyD88/NF-κB signaling.Biology direct · 2025Article
- A highland-adaptation variant near MCUR1 reduces its transcription and attenuates erythrogenesis in Tibetans.Cell genomics · 2025Article
- Case Report: A novelFrontiers in immunology · 2025Article
- A multiomic atlas identifies a treatment-resistant, bone marrow progenitor-like cell population in T cell acute lymphoblastic leukemia.Nature cancer · 2025Article
- PU.1 upregulation is linked to improved prognosis in non-small cell lung cancer.Frontiers in immunology · 2025Article
- Lentiviral vectors for precise expression to treat X-linked lymphoproliferative disease.Molecular therapy. Methods & clinical development · 2024Article
- Methylation patterns at the adjacent CpG sites within enhancers are a part of cell identity.Epigenetics & chromatin · 2024Article
5 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
3 authors at 1 institution in 1 country.
Funding
Abstract
PU.1 is an ETS-family transcription factor that plays a broad range of roles in hematopoiesis. A direct regulator of myeloid, dendritic-cell, and B cell functional programs, and a well-known antagonist of terminal erythroid cell differentiation, it is also expressed in the earliest stages of T-cell development of each cohort of intrathymic pro-T cells. Its expression in this context appears to give T-cell precursors initial, transient access to myeloid and dendritic cell developmental competence and therefore to represent a source of antagonism or delay of T-cell lineage commitment. However, it has remained uncertain until recently why T-cell development is also intensely dependent upon PU.1. Here, we review recent work that sheds light on the molecular biology of PU.1 action across the genome in pro-T cells and identifies the genes that depend on PU.1 for their correct regulation. This work indicates modes of chromatin engagement, pioneering, and cofactor recruitment ("coregulator theft") by PU.1 as well as gene network interactions that not only affect specific target genes but also have system-wide regulatory consequences, amplifying the impact of PU.1 beyond its own direct binding targets. The genes directly regulated by PU.1 also suggest a far-reaching transformation of cell biology and signaling potential between the early stages of T-cell development when PU.1 is expressed and when it is silenced. These cell-biological functions can be important to distinguish fetal from adult T-cell development and have the potential to illuminate aspects of thymic function that have so far remained the most mysterious.
Indexed as
Identifiers
What 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.