ArticleImmunity2011
Multilineage priming of enhancer repertoires precedes commitment to the B and myeloid cell lineages in hematopoietic progenitors.
Article in Immunity, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 95 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.
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
95 citing papers in PubMed, 135 citations in OpenAlex.
- Altered Postnatal Chromatin Development in the Nucleus Accumbens Primes Enduring Stress Sensitivity.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2026Article
- Transcription Activation of DEPDC1B Upon EBF1 Loss Contributes to Cell Cycle Progression and Epithelial-Mesenchymal Transition in Colon Adenocarcinoma.Biochemical genetics · 2026Article
- Echo characterizes the desynchronization of gene expression and chromatin accessibility during cell-state transitions.bioRxiv : the preprint server for biology · 2026Article
- Review
- Enhancer Trajectories in Lineage Commitment: Regulatory Logic of States and Cooperation.Biomolecules · 2026Review
- Disturbed flow-induced reprogramming of endothelial cells and two-hit mechanism of atherogenesis: transdifferentiation vs. lineage priming?Cardiovascular research · 2025Article
- Altered postnatal chromatin development in the nucleus accumbens primes lifelong stress sensitivity.bioRxiv : the preprint server for biology · 2025Article
- EnhancerNet: a predictive model of cell identity dynamics through enhancer selection.Development (Cambridge, England) · 2024Article
- Heat shock transcription factor 1 facilitates liver cancer progression by driving super-enhancer-mediated transcription of MYCN.Cancer medicine · 2024Article
- A neural network-based model framework for cell-fate decisions and development.Communications biology · 2024Article
- A landscape of gene expression regulation for synovium in arthritis.Nature communications · 2024Article
- Regularly spaced tyrosines in EBF1 mediate BRG1 recruitment and formation of nuclear subdiffractive clusters.Genes & development · 2024Article
- Tumor microenvironment restricts IL-10 induced multipotent progenitors to myeloid-lymphatic phenotype.PloS one · 2024Article
- The Function of E2A in B-Cell Development.Advances in experimental medicine and biology · 2024Review
- EBF1, PAX5, and MYC: regulation on B cell development and association with hematologic neoplasms.Frontiers in immunology · 2024Review
- Abundant binary promoter switches in lineage-determining transcription factors indicate a digital component of cell fate determination.Cell reports · 2023Article
- From Genotype to Phenotype: How Enhancers Control Gene Expression and Cell Identity in Hematopoiesis.HemaSphere · 2023Review
- Single-cell sortChIC identifies hierarchical chromatin dynamics during hematopoiesis.Nature genetics · 2023Article
- Enhancer-instructed epigenetic landscape and chromatin compartmentalization dictate a primary antibody repertoire protective against specific bacterial pathogens.Nature immunology · 2023Article
- Unveiling the complexity of transcription factor networks in hematopoietic stem cells: implications for cell therapy and hematological malignancies.Frontiers in oncology · 2023Review
35 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
10 authors at 2 institutions in 2 countries.
Funding
Abstract
Recent studies have documented genome-wide binding patterns of transcriptional regulators and their associated epigenetic marks in hematopoietic cell lineages. In order to determine how epigenetic marks are established and maintained during developmental progression, we have generated long-term cultures of hematopoietic progenitors by enforcing the expression of the E-protein antagonist Id2. Hematopoietic progenitors that express Id2 are multipotent and readily differentiate upon withdrawal of Id2 expression into committed B lineage cells, thus indicating a causative role for E2A (Tcf3) in promoting the B cell fate. Genome-wide analyses revealed that a substantial fraction of lymphoid and myeloid enhancers are premarked by the poised or active enhancer mark H3K4me1 in multipotent progenitors. Thus, in hematopoietic progenitors, multilineage priming of enhancer elements precedes commitment to the lymphoid or myeloid cell lineages.
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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.