ArticleMolecular and cellular biology1993
The human beta fibrinogen promoter contains a hepatocyte nuclear factor 1-dependent interleukin-6-responsive element.
Article in Molecular and cellular biology, 1993. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers, 1 of them a synthesis that pooled it.
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Who cites it
27 citing papers in PubMed, 1 synthesis or guideline pooled it, 147 citations in OpenAlex.
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- Curcuma longa extract improves serum inflammatory markers and mental health in healthy participants who are overweight: a randomized, double-blind, placebo-controlled trial.Nutrition journal · 2021Trial
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- Regulation of fibrinogen synthesis.Thrombosis research · 2024Review
- Human gain-of-function variants in HNF1A confer protection from diabetes but independently increase hepatic secretion of atherogenic lipoproteins.Cell genomics · 2023Article
- Immunoglobulin G N-glycan, inflammation and type 2 diabetes in East Asian and European populations: a Mendelian randomization study.Molecular medicine (Cambridge, Mass.) · 2022Article
- The Role of C-Reactive Protein and Fibrinogen in the Development of Intracerebral Hemorrhage: A Mendelian Randomization Study in European Population.Frontiers in genetics · 2021Article
- Polymorphisms -455G/A and -148C/T and Fibrinogen Plasmatic Level as Risk Markers of Coronary Disease and Major Adverse Cardiovascular Events.Disease markers · 2019Article
- Hepatocytes: a key cell type for innate immunity.Cellular & molecular immunology · 2016Review
- Pleiotropic effects of HNF1A rs1183910 in a population-based study of 60,283 individuals.Diabetologia · 2014Article
- Interleukin-6 promotor polymorphisms and coronary vasospastic angina in Han Chinese.International journal of clinical and experimental medicine · 2014Article
- CYLD enhances severe listeriosis by impairing IL-6/STAT3-dependent fibrin production.PLoS pathogens · 2013Article
- Fibrinogen as a key regulator of inflammation in disease.Seminars in immunopathology · 2012Review
- Interaction between fibrinogen and IL-6 genetic variants and associations with cardiovascular disease risk in the Cardiovascular Health Study.Annals of human genetics · 2010Article
- Modification of the interleukin-6 response to air pollution by interleukin-6 and fibrinogen polymorphisms.Environmental health perspectives · 2009Article
- Ischemic stroke risk, smoking, and the genetics of inflammation in a biracial population: the stroke prevention in young women study.Thrombosis journal · 2008Article
- Roles of IL-6-gp130 Signaling in Vascular Inflammation.Current cardiology reviews · 2008Article
- Analysis of G(-174)C IL-6 polymorphism and plasma concentrations of inflammatory markers in patients with type 2 diabetes and peripheral arterial disease.Journal of clinical pathology · 2006Article
- The -174 G/C polymorphism of the interleukin-6 gene promoter and essential hypertension in an elderly Italian population.Journal of human hypertension · 2002Article
- Essential role of STAT3 in the control of the acute-phase response as revealed by inducible gene inactivation [correction of activation] in the liver.Molecular and cellular biology · 2001Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Acute-phase reactants are liver proteins whose synthesis is positively or negatively regulated during inflammation. The main mediators of this phenomenon are glucocorticoids and interleukin-6 (IL-6), a pleiotropic cytokine that also controls hematopoiesis. Functional analysis of several acute-phase reactant promoter regions has identified two major DNA motifs used by IL-6-regulated genes. The first one corresponds to a CTGG(G/A)AA sequence, and the other is a binding site for members of the C/EBP family of nuclear proteins. We have previously shown that the human beta fibrinogen (beta Fg) promoter contains an IL-6-responsive region, located between bp -150 and -67 (P. Huber, M. Laurent, and J. Dalmon, J. Biol. Chem. 265:5695-5701, 1990). In this study, using DNase I footprinting, mobility shift assays, and mutagenesis, we demonstrate that at least three subdomains of this region are necessary to observe a full response to IL-6. The most distal contains a CTGGGAA motif, and its mutation inhibits IL-6 stimulation. Another, which is able to interact with several distinct nuclear proteins, among them members of the C/EBP family, is dispensable for IL-6 induction but plays an important role in the constitutive expression of beta Fg. Finally, a proximal hepatocyte nuclear factor 1 binding site, already described as the major determinant of beta Fg tissue-specific expression, is also required for IL-6 stimulation. These results indicate a complex interplay between nuclear proteins within the beta Fg IL-6-responsive region and suggest a tight functional coupling between the tissue-specific and inducible elements.
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