ArticleProceedings of the National Academy of Sciences of the United States of America1996
The Gfi-1 protooncoprotein represses Bax expression and inhibits T-cell death.
Article in Proceedings of the National Academy of Sciences of the United States of America, 1996. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.
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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
47 citing papers in PubMed, 103 citations in OpenAlex.
- Mechanisms of HIV Latency in Hematopoietic Progenitors: GFI1 as a Key Regulator.bioRxiv : the preprint server for biology · 2026Article
- CHD3 and CHD4 coordinate gene expression programs to maintain β-cell function and identityResearch square · 2025Article
- GFI1 promotes the proliferation and migration of esophageal squamous cell carcinoma cells through the inhibition of SOCS1 expression.International journal of molecular medicine · 2021Article
- Epigenetic regulation in medulloblastoma pathogenesis revealed by genetically engineered mouse models.Cancer science · 2021Review
- GFI-1 overexpression promotes cell proliferation and apoptosis resistance in mycosis fungoides by repressing Bax and P21.Oncology letters · 2021Article
- Cigarette smoke-induced alterations in blood: A review of research on DNA methylation and gene expression.Experimental and clinical psychopharmacology · 2021Review
- Gfi1 upregulates c-Myc expression and promotes c-Myc-driven cell proliferation.Scientific reports · 2020Article
- A novel regulatory circuit between p53 and GFI1 controls induction of apoptosis in T cells.Scientific reports · 2019Article
- Lsd1 as a therapeutic target in Gfi1-activated medulloblastoma.Nature communications · 2019Article
- microRNA-22 promotes megakaryocyte differentiation through repression of its target,Blood advances · 2019Article
- Growth factor independence 1 expression in myeloma cells enhances their growth, survival, and osteoclastogenesis.Journal of hematology & oncology · 2018Article
- GFI1 facilitates efficient DNA repair by regulating PRMT1 dependent methylation of MRE11 and 53BP1.Nature communications · 2018Article
- Article
- EZH2 or HDAC1 Inhibition Reverses Multiple Myeloma-Induced Epigenetic Suppression of Osteoblast Differentiation.Molecular cancer research : MCR · 2017Article
- Transcription factors and target genes of pre-TCR signaling.Cellular and molecular life sciences : CMLS · 2015Review
- Snail/Gfi-1 (SNAG) family zinc finger proteins in transcription regulation, chromatin dynamics, cell signaling, development, and disease.Cytokine & growth factor reviews · 2013Review
- Article
- Growth factor independent-1 maintains Notch1-dependent transcriptional programming of lymphoid precursors.PLoS genetics · 2013Article
- The transcription factor Lyl-1 regulates lymphoid specification and the maintenance of early T lineage progenitors.Nature immunology · 2012Article
- The enhancer of trithorax and polycomb gene Caf1/p55 is essential for cell survival and patterning in Drosophila development.Development (Cambridge, England) · 2011Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
Abstract
The Gfi-1 protooncogene encodes a nuclear zinc-finger protein that carries a novel repressor domain, SNAG, and functions as a position- and orientation-independent active transcriptional repressor. The Gfi-1 repressor allows interleukin 2 (IL-2)-dependent T cells to escape G1 arrest induced by IL-2 withdrawal in culture and collaborates with c-myc and pim-1 for the induction of retrovirus-induced lymphomas in animals. Here we show that overexpression of Gfi-1 also inhibits cell death induced by cultivation of IL-2-dependent T-cell lines in IL-2-deficient media. Similarly, induction of Gfi-1 in primary thymocytes from mice carrying a metal-inducible Gfi-1 transgene inhibits cell death induced by cultivation in vitro. The protein and mRNA levels of the proapoptotic regulator Bax are down-regulated by Gfi-1 in both immortalized T-cell lines and primary transgenic thymocytes. The repression is direct and depends on several Gfi-1-binding sites in the p53-inducible Bax promoter. In addition to Bax, Gfi-1 also represses Bak, another apoptosis-promoting member of the Bcl-2 gene family. Therefore, Gfi-1 may inhibit apoptosis by means of its repression of multiple proapoptotic regulators. The antiapoptotic properties of Gfi-1 provide a potential explanation for its strong collaboration with c-myc during oncogenesis.
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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.