ArticleNature immunology2016
Asynchronous combinatorial action of four regulatory factors activates Bcl11b for T cell commitment.
Article in Nature immunology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 99 papers.
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Who cites it
99 citing papers in PubMed, 141 citations in OpenAlex.
- Bcl11b dose-dependently regulates positive selection of CD8 T cells to the virtual memory fate.bioRxiv : the preprint server for biology · 2026Article
- APOBEC2 deficiency disrupts hematopoietic lineage commitment, resulting in emergence of dual identity lymphocytes in mice and humans.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- T cell development from expanded hematopoietic progenitors reveals initiation control byScience immunology · 2026Article
- Enhancer Trajectories in Lineage Commitment: Regulatory Logic of States and Cooperation.Biomolecules · 2026Review
- Upregulation of CD90 correlates with T lineage commitment at the DN2a stage of T cell development.Frontiers in immunology · 2026Article
- The epigenetic landscape of fate decisions in T cells.Nature immunology · 2025Review
- Disruption of Notch signaling by KGF induces a developmental pause in thymocytes.Frontiers in immunology · 2025Article
- Activation-derepression synergy enables a bHLH network to coordinate a signal-specific fate response.Cell reports · 2024Article
- A timed epigenetic switch balances T and ILC lineage proportions in the thymus.Development (Cambridge, England) · 2024Article
- TCF1 dosage determines cell fate during T cell development.Science advances · 2024Article
- Transcriptional network dynamics in early T cell development.The Journal of experimental medicine · 2024Review
- Pivotal role of BCL11B in the immune, hematopoietic and nervous systems: a review of the BCL11B-associated phenotypes from the genetic perspective.Genes and immunity · 2024Review
- Transcriptional priming and chromatin regulation during stochastic cell fate specification.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2024Review
- T-cell commitment inheritance-an agent-based multi-scale model.NPJ systems biology and applications · 2024Article
- Reversible, tunable epigenetic silencing of TCF1 generates flexibility in the T cell memory decision.Immunity · 2024Article
- The multifaceted roles of TCF1 in innate and adaptive lymphocytes.Advances in immunology · 2024Review
- T-cell commitment inheritance - an agent-based multi-scale model.bioRxiv : the preprint server for biology · 2023Article
- Three-dimensional genome structure and function.MedComm · 2023Review
- T cells in health and disease.Signal transduction and targeted therapy · 2023Review
- Speed and navigation control of thymocyte development by the fetal T-cell gene regulatory network.Immunological reviews · 2023Review
39 more citing papers are in PubMed but not listed here.
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Authors and funding
11 authors at 2 institutions in 1 country.
Funding
Abstract
During T cell development, multipotent progenitors relinquish competence for other fates and commit to the T cell lineage by turning on Bcl11b, which encodes a transcription factor. To clarify lineage commitment mechanisms, we followed developing T cells at the single-cell level using Bcl11b knock-in fluorescent reporter mice. Notch signaling and Notch-activated transcription factors collaborate to activate Bcl11b expression irrespectively of Notch-dependent proliferation. These inputs work via three distinct, asynchronous mechanisms: an early locus 'poising' function dependent on TCF-1 and GATA-3, a stochastic-permissivity function dependent on Notch signaling, and a separate amplitude-control function dependent on Runx1, a factor already present in multipotent progenitors. Despite their necessity for Bcl11b expression, these inputs act in a stage-specific manner, providing a multitiered mechanism for developmental gene regulation.
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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.