ArticleThe Biochemical journal2004
Nuclear factor-kappaB motif and interferon-alpha-stimulated response element co-operate in the activation of guanylate-binding protein-1 expression by inflammatory cytokines in endothelial cells.
Article in The Biochemical journal, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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Who cites it
33 citing papers in PubMed, 76 citations in OpenAlex.
- The transcription factor RIP140 regulates interferon γ signaling in breast cancer.International journal of cancer · 2025Article
- Review
- Human GBP1 Is Involved in the Repair of Damaged Phagosomes/Endolysosomes.International journal of molecular sciences · 2023Article
- Identifying the key genes of Epstein-Barr virus-regulated tumour immune microenvironment of gastric carcinomas.Cell proliferation · 2023Article
- Role of biomarkers in the diagnosis and prognosis of patients with cutaneous lupus erythematosus.Annals of translational medicine · 2021Review
- Comprehensive Analysis of the Expression and Prognosis for GBPs in Head and neck squamous cell carcinoma.Scientific reports · 2020Article
- Article
- Interferon-induced guanylate-binding proteins: Guardians of host defense in health and disease.The Journal of experimental medicine · 2019Review
- Guanylate-Binding Protein 1: An Emerging Target in Inflammation and Cancer.Frontiers in immunology · 2019Review
- Genome-Wide Inhibition of Pro-atherogenic Gene Expression by Multi-STAT Targeting Compounds as a Novel Treatment Strategy of CVDs.Frontiers in immunology · 2018Article
- Processing and secretion of guanylate binding protein-1 depend on inflammatory caspase activity.Journal of cellular and molecular medicine · 2017Article
- Guanylate-Binding Protein 1 Inhibits Nuclear Delivery of Kaposi's Sarcoma-Associated Herpesvirus Virions by Disrupting Formation of Actin Filament.Journal of virology · 2017Article
- Viral IL-10 down-regulates the "MHC-I antigen processing operon" through the NF-κB signaling pathway in nasopharyngeal carcinoma cells.Cytotechnology · 2016Article
- Structural proteins of Kaposi's sarcoma-associated herpesvirus antagonize p53-mediated apoptosis.Oncogene · 2015Article
- Resveratrol inhibits dysfunction of dendritic cells from chronic obstructive pulmonary disease patients through promoting miR-34.International journal of clinical and experimental pathology · 2015Article
- Gamma interferon-induced guanylate binding protein 1 is a novel actin cytoskeleton remodeling factor.Molecular and cellular biology · 2014Article
- STAT1-dependent signal integration between IFNγ and TLR4 in vascular cells reflect pro-atherogenic responses in human atherosclerosis.PloS one · 2014Article
- Human T cell leukemia virus type I tax-induced IκB-ζ modulates tax-dependent and tax-independent gene expression in T cells.Neoplasia (New York, N.Y.) · 2013Article
- Multiple interferon regulatory factor and NF-κB sites cooperate in mediating cell-type- and maturation-specific activation of the human CD83 promoter in dendritic cells.Molecular and cellular biology · 2013Article
- Microarray analyses of genes regulated by isoflurane anesthesia in vivo: a novel approach to identifying potential preconditioning mechanisms.Anesthesia and analgesia · 2013Article
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The large GTPase GBP-1 (guanylate-binding protein-1) is a major IFN-gamma (interferon-gamma)-induced protein with potent anti-angiogenic activity in endothelial cells. An ISRE (IFN-alpha-stimulated response element) is necessary and sufficient for the induction of GBP-1 expression by IFN-gamma. Recently, we have shown that in vivo GBP-1 expression is strongly endothelial-cell-associated and is, in addition to IFN-gamma, also activated by interleukin-1beta and tumour necrosis factor-alpha, both in vitro and in vivo [Lubeseder-Martellato, Guenzi, Jörg, Töpolt, Naschberger, Kremmer, Zietz, Tschachler, Hutzler, Schwemmle et al. (2002) Am. J. Pathol. 161, 1749-1759; Guenzi, Töpolt, Cornali, Lubeseder-Martellato, Jörg, Matzen, Zietz, Kremmer, Nappi, Schwemmle et al. (2001) EMBO J. 20, 5568-5577]. In the present study, we identified a NF-kappaB (nuclear factor kappaB)-binding motif that, together with ISRE, is required for the induction of GBP-1 expression by interleukin-1beta and tumour necrosis factor-alpha. Deactivation of the NF-kappaB motif reduced the additive effects of combinations of these cytokines with IFN-gamma by more than 50%. Importantly, NF-kappaB p50 rather than p65 activated the GBP-1 promoter. The NF-kappaB motif and ISRE were detected in an almost identical spatial organization, as in the GBP-1 promoter, in the promoter regions of various inflammation-associated genes. Therefore both motifs may constitute a cooperative inflammatory cytokine response module that regulates GBP-1 expression. Our findings may open new perspectives for the use of NF-kappaB inhibitors to support angiogenesis in inflammatory diseases including ischaemia.
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