ArticleMolecular and cellular biology2010
Zinc finger protein Gfi1 controls the endotoxin-mediated Toll-like receptor inflammatory response by antagonizing NF-kappaB p65.
Article in Molecular and cellular biology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 34 citations in OpenAlex.
- Alginate oligosaccharide indirectly affects toll-like receptor signaling via the inhibition of microRNA-29b in aneurysm patients after endovascular aortic repair.Drug design, development and therapy · 2017Trial
- Tobacco Smoke Exposure From Prenatal To Adolescent Periods Drives IBD Pathogenesis: Dynamic DNA Methylation Signatures Across Lifespan Stages.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Mechanisms of HIV Latency in Hematopoietic Progenitors: GFI1 as a Key Regulator.bioRxiv : the preprint server for biology · 2026Article
- Agonism of GPR84 Attenuates Free Fatty Acid-Induced Endothelial Inflammation and Monocyte Adhesion via Gfi1/NF-κB Pathway.Arquivos brasileiros de cardiologia · 2026Article
- Spatiotemporal proteomic profiling of the pro-inflammatory response to lipopolysaccharide in the THP-1 human leukaemia cell line.Nature communications · 2021Article
- Chronic stress primes innate immune responses in mice and humans.Cell reports · 2021Article
- PARP Traps Rescue the Pro-Inflammatory Response of Human Macrophages in the In Vitro Model of LPS-Induced Tolerance.Pharmaceuticals (Basel, Switzerland) · 2021Article
- GFI-1 Protects Against Lipopolysaccharide-Induced Inflammatory Responses and Apoptosis by Inhibition of the NF-κB/TNF-α Pathway in H9c2 Cells.Inflammation · 2020Article
- Whole Genome Microarray Analysis of DUSP4-Deletion Reveals A Novel Role for MAP Kinase Phosphatase-2 (MKP-2) in Macrophage Gene Expression and Function.International journal of molecular sciences · 2019Article
- Combating viral contaminants in CHO cells by engineering innate immunity.Scientific reports · 2019Article
- EZH2 or HDAC1 Inhibition Reverses Multiple Myeloma-Induced Epigenetic Suppression of Osteoblast Differentiation.Molecular cancer research : MCR · 2017Article
- Acute myeloid leukemia cells polarize macrophages towards a leukemia supporting state in a Growth factor independence 1 dependent manner.Haematologica · 2016Article
- Next-generation profiling to identify the molecular etiology of Parkinson dementia.Neurology. Genetics · 2016Article
- Article
- Zinc finger protein 64 promotes Toll-like receptor-triggered proinflammatory and type I interferon production in macrophages by enhancing p65 subunit activation.The Journal of biological chemistry · 2013Article
- Zinc finger protein ZBTB20 promotes Toll-like receptor-triggered innate immune responses by repressing IκBα gene transcription.Proceedings of the National Academy of Sciences of the United States of America · 2013Article
- Zinc in innate and adaptive tumor immunity.Journal of translational medicine · 2010Review
Corrections and comments
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Authors and funding
12 authors at 5 institutions in 4 countries.
Funding
Abstract
Endotoxin (bacterial lipopolysaccharide [LPS]) causes fatal septic shock via the Toll-like receptor 4 (TLR-4) protein present on innate immunity effector cells, which activates nuclear factor kappa B (NF-kappaB), inducing proinflammatory cytokines, including tumor necrosis factor alpha (TNF-alpha). An early step in this process involves nuclear sequestration of the p65-RelA NF-kappaB subunit, enabling transcriptional activation of target inflammatory cytokine genes. Here, we analyzed the role of the nuclear zinc finger protein Gfi1 in the TLR response using primary bone marrow-derived macrophages. We show that upon LPS stimulation, expression of Gfi1 is induced with kinetics similar to those of nuclear translocation of p65 and that Gfi1 interacts with p65 and inhibits p65-mediated transcriptional transactivation by interfering with p65 binding to target gene promoter DNA. Gfi1-deficient macrophages show abnormally high mRNA levels of the TNF-alpha gene and many other p65 target genes and a higher rate of TNF promoter occupancy by p65 than wild-type cells after LPS stimulation, suggesting that Gfi1 functions as an antagonist of NF-kappaB activity at the level of promoter binding. Our findings identify a new function of Gfi1 as a general negative regulator of the endotoxin-initiated innate immune responses, including septic shock and possibly other severe inflammatory diseases.
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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.