ArticlePloS one2016
Threshold Levels of Gfi1 Maintain E2A Activity for B Cell Commitment via Repression of Id1.
Article in PloS one, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 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
10 citing papers in PubMed, 15 citations in OpenAlex.
- GFI1 as a novel regulator of γδ T cell development and the IL-17/IFN-γ lineage commitment.Frontiers in immunology · 2026Article
- Immune cell-resolved transcriptomics provides insights into the basis for variations of fish genetic resistance to viral disease.BMC biology · 2025Article
- ID1 in hematopoiesis and hematologic disorders: novel potentials of a classic differentiation regulator.Cellular & molecular biology letters · 2025Review
- GFI1-Dependent Repression ofCancers · 2022Article
- Enhancer jungles establish robust tissue-specific regulatory control in the human genome.Genomics · 2020Article
- Multifaceted Actions of GFI1 and GFI1B in Hematopoietic Stem Cell Self-Renewal and Lineage Commitment.Frontiers in genetics · 2020Review
- A novel regulatory circuit between p53 and GFI1 controls induction of apoptosis in T cells.Scientific reports · 2019Article
- Reduced expression but not deficiency of GFI1 causes a fatal myeloproliferative disease in mice.Leukemia · 2019Article
- GFI1 facilitates efficient DNA repair by regulating PRMT1 dependent methylation of MRE11 and 53BP1.Nature communications · 2018Article
- Obesity alters the long-term fitness of the hematopoietic stem cell compartment through modulation ofThe Journal of experimental medicine · 2018Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
A regulatory circuit that controls myeloid versus B lymphoid cell fate in hematopoietic progenitors has been proposed, in which a network of the transcription factors Egr1/2, Nab, Gfi1 and PU.1 forms the core element. Here we show that a direct link between Gfi1, the transcription factor E2A and its inhibitor Id1 is a critical element of this regulatory circuit. Our data suggest that a certain threshold of Gfi1 is required to gauge E2A activity by adjusting levels of Id1 in multipotent progenitors, which are the first bipotential myeloid/lymphoid-restricted progeny of hematopoietic stem cells. If Gfi1 levels are high, Id1 is repressed enabling E2A to activate a specific set of B lineage genes by binding to regulatory elements for example the IL7 receptor gene. If Gfi1 levels fall below a threshold, Id1 expression increases and renders E2A unable to function, which prevents hematopoietic progenitors from engaging along the B lymphoid lineage.
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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.