ArticleDevelopment (Cambridge, England)2013
Architecture of a lymphomyeloid developmental switch controlled by PU.1, Notch and Gata3.
Article in Development (Cambridge, England), 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 64 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
64 citing papers in PubMed, 95 citations in OpenAlex.
- Animals have expanded the evolutionary legacy of unicellular ancestors in blood cells.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Article
- T Cell Development: From T-Lineage Specification to Intrathymic Maturation.Advances in experimental medicine and biology · 2025Review
- Ever-evolving insights into the cellular and molecular drivers of lymphoid cell development.Experimental hematology · 2024Review
- Transcriptional network dynamics in early T cell development.The Journal of experimental medicine · 2024Review
- T-cell commitment inheritance-an agent-based multi-scale model.NPJ systems biology and applications · 2024Article
- Distinct use of super-enhancer elements controls cell type-specific CD25 transcription and function.Science immunology · 2023Article
- T-cell commitment inheritance - an agent-based multi-scale model.bioRxiv : the preprint server for biology · 2023Article
- Speed and navigation control of thymocyte development by the fetal T-cell gene regulatory network.Immunological reviews · 2023Review
- Review
- Multi-lineage Differentiation from Hematopoietic Stem Cells.Advances in experimental medicine and biology · 2023Review
- Multi-modular structure of the gene regulatory network for specification and commitment of murine T cells.Frontiers in immunology · 2023Review
- Single-cell deletion analyses show control of pro-T cell developmental speed and pathways by Tcf7, Spi1, Gata3, Bcl11a, Erg, and Bcl11b.Science immunology · 2022Article
- Article
- Interleukin-7 receptor signaling is crucial for enhancer-dependent TCRδ germline transcription mediated through STAT5 recruitment.Frontiers in immunology · 2022Article
- Shifting gears: Id3 enables recruitment of E proteins to new targets during T cell development and differentiation.Frontiers in immunology · 2022Review
- Logic and lineage impacts on functional transcription factor deployment for T-cell fate commitment.Biophysical journal · 2021Review
- Oncogenic cooperation between TCF7-SPI1 and NRAS(G12D) requires β-catenin activity to drive T-cell acute lymphoblastic leukemia.Nature communications · 2021Article
- The Route of Early T Cell Development: Crosstalk between Epigenetic and Transcription Factors.Cells · 2021Review
- How transcription factors drive choice of the T cell fate.Nature reviews. Immunology · 2021Review
4 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
2 authors at 1 institution in 1 country.
Funding
Abstract
Hematopoiesis is a classic system with which to study developmental potentials and to investigate gene regulatory networks that control choices among alternate lineages. T-cell progenitors seeding the thymus retain several lineage potentials. The transcription factor PU.1 is involved in the decision to become a T cell or a myeloid cell, and the developmental outcome of expressing PU.1 is dependent on exposure to Notch signaling. PU.1-expressing T-cell progenitors without Notch signaling often adopt a myeloid program, whereas those exposed to Notch signals remain in a T-lineage pathway. Here, we show that Notch signaling does not alter PU.1 transcriptional activity by degradation/alteration of PU.1 protein. Instead, Notch signaling protects against the downregulation of T-cell factors so that a T-cell transcriptional network is maintained. Using an early T-cell line, we describe two branches of this network. The first involves inhibition of E-proteins by PU.1 and the resulting inhibition of Notch signaling target genes. Effects of E-protein inhibition can be reversed by exposure to Notch signaling. The second network is dependent on the ability of PU.1 to inhibit important T-cell transcription factor genes such as Myb, Tcf7 and Gata3 in the absence of Notch signaling. We show that maintenance of Gata3 protein levels by Myb and Notch signaling is linked to the ability to retain T-cell identity in response to PU.1.
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.