ArticleOncogene2007
Cooperative interaction between ETS1 and GFI1 transcription factors in the repression of Bax gene expression.
Article in Oncogene, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 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
16 citing papers in PubMed, 39 citations in OpenAlex.
- Brief research report: ETS-1 blockade increases ICAM-1 expression in activated human retinal endothelial cells.Frontiers in ophthalmology · 2024Article
- Growth Factor Independence 1B-Mediated Transcriptional Repression and Lineage Allocation Require Lysine-Specific Demethylase 1-Dependent Recruitment of the BHC Complex.Molecular and cellular biology · 2019Article
- miR‑512‑5p suppresses proliferation, migration and invasion, and induces apoptosis in non‑small cell lung cancer cells by targeting ETS1.Molecular medicine reports · 2019Article
- Bcl-xScientific reports · 2019Article
- Growth factor independence 1 expression in myeloma cells enhances their growth, survival, and osteoclastogenesis.Journal of hematology & oncology · 2018Article
- PC-TraFF: identification of potentially collaborating transcription factors using pointwise mutual information.BMC bioinformatics · 2015Article
- ETS1 is a genome-wide effector of RAS/ERK signaling in epithelial cells.Nucleic acids research · 2014Article
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- Abnormal expression of FLI1 protein is an adverse prognostic factor in acute myeloid leukemia.Blood · 2011Article
- Gfi1 and Gfi1b: key regulators of hematopoiesis.Leukemia · 2010Review
- Gfi-1 represses CDKN2B encoding p15INK4B through interaction with Miz-1.Proceedings of the National Academy of Sciences of the United States of America · 2009Article
- Ets1 induces dysplastic changes when expressed in terminally-differentiating squamous epidermal cells.PloS one · 2009Article
- Formation of IL-7Ralphahigh and IL-7Ralphalow CD8 T cells during infection is regulated by the opposing functions of GABPalpha and Gfi-1.Journal of immunology (Baltimore, Md. : 1950) · 2008Article
- Genetic heterogeneity in severe congenital neutropenia: how many aberrant pathways can kill a neutrophil?Current opinion in allergy and clinical immunology · 2007Review
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 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The proto-oncoproteins ETS1 and growth factor independent-1 (GFI1) are implicated in cell growth and differentiation in various types of cells, and their deregulated expression is involved in malignant transformation. Here, we report that ETS1 and GFI1 interact and affect gene expression through their cross-talk. Co-immunoprecipitation analyses and glutathione-S-transferase pull-down assays revealed that ETS1 bound directly to GFI1 via its Ets domain, and GFI1 bound to ETS1 via its zinc-finger domain. Luciferase (Luc) assays using artificial reporters showed that GFI1 repressed ETS1-mediated transcriptional activation and ETS1 repressed GFI1-mediated transcriptional activation, in a dose-dependent manner. However, in the Bax promoter where the Ets- and Gfi-binding sites (EBS and GBS) are adjacent, ETS1 and GFI1 cooperatively reduced activation. Site-directed mutagenesis on the EBS and GBS of the Bax promoter showed that both binding sites were necessary for full repression. Chromatin immunoprecipitation analyses confirmed that an ETS1-GFI1 complex formed on the Bax promoter even when either EBS or GBS was mutated. Introduction of small interfering RNA against ETS1 and/or GFI1 enhanced endogenous Bax gene expression. Our results suggest that the interaction between ETS1 and GFI1 facilitates their binding to specific sites on the Bax promoter and represses Bax expression in vivo.
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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.