ArticleMolecular and cellular biology1996
The Gfi-1 proto-oncoprotein contains a novel transcriptional repressor domain, SNAG, and inhibits G1 arrest induced by interleukin-2 withdrawal.
Article in Molecular and cellular biology, 1996. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 131 papers.
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Who cites it
131 citing papers in PubMed, 272 citations in OpenAlex.
- Mechanisms of HIV Latency in Hematopoietic Progenitors: GFI1 as a Key Regulator.bioRxiv : the preprint server for biology · 2026Article
- GFI1 as a novel regulator of γδ T cell development and the IL-17/IFN-γ lineage commitment.Frontiers in immunology · 2026Article
- GFI1-driven transcriptional and epigenetic programs maintain CD8Nature immunology · 2025Article
- Gfi1 controls the formation of effector-like CD8Nature communications · 2025Article
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- An "unexpected" role for EMT transcription factors in hematological development and malignancy.Frontiers in immunology · 2023Review
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- Review
- GFI1 Cooperates with IKZF1/IKAROS to Activate Gene Expression in T-cell Acute Lymphoblastic Leukemia.Molecular cancer research : MCR · 2022Article
- Presence of theFrontiers in oncology · 2022Article
- Repurposing the lineage-determining transcription factor Atoh1 without redistributing its genomic binding sites.Frontiers in cell and developmental biology · 2022Article
- Irf2bp2a regulates terminal granulopoiesis through proteasomal degradation of Gfi1aa in zebrafish.PLoS genetics · 2021Article
- GFI-1 overexpression promotes cell proliferation and apoptosis resistance in mycosis fungoides by repressing Bax and P21.Oncology letters · 2021Article
- Involvement of Scratch2 in GalR1-mediated depression-like behaviors in the rat ventral periaqueductal gray.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- The Post-Translational Regulation of Epithelial-Mesenchymal Transition-Inducing Transcription Factors in Cancer Metastasis.International journal of molecular sciences · 2021Review
- The role of epithelial-mesenchymal transition-regulating transcription factors in anti-cancer drug resistance.Archives of pharmacal research · 2021Review
- LSD1: more than demethylation of histone lysine residues.Experimental & molecular medicine · 2020Review
- Gfi1 upregulates c-Myc expression and promotes c-Myc-driven cell proliferation.Scientific reports · 2020Article
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71 more citing papers are in PubMed but not listed here.
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
The Gfi-1 proto-oncogene is activated by provirus insertion in T-cell lymphoma lines selected for interleukin-2 (IL-2) independence in culture and in primary retrovirus-induced thymomas and encodes a nuclear, sequence-specific DNA-binding protein. Here we show that Gfi-1 is a position- and orientation-independent active transcriptional repressor, whose activity depends on a 20-amino-acid N-terminal repressor domain, coincident with a nuclear localization motif. The sequence of the Gfi-1 repressor domain is related to the sequence of the repressor domain of Gfi-1B, a Gfi-1-related protein, and to sequences at the N termini of the insulinoma-associated protein, IA-1, the homeobox protein Gsh-1, and the vertebrate but not the Drosophila members of the Snail-Slug protein family (Snail/Gfi-1, SNAG domain). Although not functionally characterized, these SNAG-related sequences are also likely to mediate transcriptional repression. Therefore, the Gfi-1 SNAG domain may be the prototype of a novel family of evolutionarily conserved repressor domains that operate in multiple cell lineages. Gfi-1 overexpression in IL-2-dependent T-cell lines allows the cells to escape from the G1 arrest induced by IL-2 withdrawal. Since a single point mutation in the SNAG domain (P2A) inhibits both the Gfi-1-mediated transcriptional repression and the G1 arrest induced by IL-2 starvation, we conclude that the latter depends on the repressor activity of the SNAG domain. Induction of Gfi-1 may therefore contribute to T-cell activation and tumor progression by repressing the expression of genes that inhibit cellular proliferation.
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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.