ArticlePLoS genetics2013
Growth factor independent-1 maintains Notch1-dependent transcriptional programming of lymphoid precursors.
Article in PLoS genetics, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 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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Who cites it
18 citing papers in PubMed, 25 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
- Associations Between Non-Genetic Risk Factors and DNA Methylation Alterations in Barrett's Esophagus and Its Progression to Esophageal Adenocarcinoma.International journal of molecular sciences · 2025Review
- Transcriptional network dynamics in early T cell development.The Journal of experimental medicine · 2024Review
- Dose-dependent effect of GFI1 expression in the reconstitution and the differentiation capacity of HSCs.Frontiers in cell and developmental biology · 2023Article
- Multi-modular structure of the gene regulatory network for specification and commitment of murine T cells.Frontiers in immunology · 2023Review
- How transcription factors drive choice of the T cell fate.Nature reviews. Immunology · 2021Review
- Multifaceted Actions of GFI1 and GFI1B in Hematopoietic Stem Cell Self-Renewal and Lineage Commitment.Frontiers in genetics · 2020Review
- Temporal Expression of Bim Limits the Development of Agonist-Selected Thymocytes and Skews Their TCRβ Repertoire.Journal of immunology (Baltimore, Md. : 1950) · 2017Article
- The ubiquitin ligase Huwe1 regulates the maintenance and lymphoid commitment of hematopoietic stem cells.Nature immunology · 2016Article
- Article
- Global DNA methylation patterns in Barrett's esophagus, dysplastic Barrett's, and esophageal adenocarcinoma are associated with BMI, gender, and tobacco use.Clinical epigenetics · 2016Article
- Forging T-Lymphocyte Identity: Intersecting Networks of Transcriptional Control.Advances in immunology · 2016Review
- Review
- Transcription factors and target genes of pre-TCR signaling.Cellular and molecular life sciences : CMLS · 2015Review
- Growth Factor Independence-1 (Cellular and molecular gastroenterology and hepatology · 2015Article
- SCL, LMO1 and Notch1 reprogram thymocytes into self-renewing cells.PLoS genetics · 2014Article
- Shared mechanisms between Drosophila peripheral nervous system development and human neurodegenerative diseases.Current opinion in neurobiology · 2014Review
- Developmental gene networks: a triathlon on the course to T cell identity.Nature reviews. Immunology · 2014Review
Corrections and comments
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Authors and funding
11 authors at 5 institutions in 3 countries.
Funding
Abstract
Growth factor independent 1 (Gfi1) is a transcriptional repressor originally identified as a gene activated in T-cell leukemias induced by Moloney-murine-leukemia virus infection. Notch1 is a transmembrane receptor that is frequently mutated in human T-cell acute lymphoblastic leukemia (T-ALL). Gfi1 is an important factor in the initiation and maintenance of lymphoid leukemias and its deficiency significantly impedes Notch dependent initiation of T-ALL in animal models. Here, we show that immature hematopoietic cells require Gfi1 to competently integrate Notch-activated signaling. Notch1 activation coupled with Gfi1 deficiency early in T-lineage specification leads to a dramatic loss of T-cells, whereas activation in later stages leaves development unaffected. In Gfi1 deficient multipotent precursors, Notch activation induces lethality and is cell autonomous. Further, without Gfi1, multipotent progenitors do not maintain Notch1-activated global expression profiles typical for T-lineage precursors. In agreement with this, we find that both lymphoid-primed multipotent progenitors (LMPP) and early T lineage progenitors (ETP) do not properly form or function in Gfi1(-/-) mice. These defects correlate with an inability of Gfi1(-/-) progenitors to activate lymphoid genes, including IL7R, Rag1, Flt3 and Notch1. Our data indicate that Gfi1 is required for hematopoietic precursors to withstand Notch1 activation and to maintain Notch1 dependent transcriptional programming to determine early T-lymphoid lineage identity.
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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.