ArticleNucleic acids research1992
Cooperative effects of C/EBP-like and NF kappa B-like binding sites on rat serum amyloid A1 gene expression in liver cells.
Article in Nucleic acids research, 1992. 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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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
17 citing papers in PubMed, 74 citations in OpenAlex.
- SAA4: An Underdog Within the Serum Amyloid a Superfamily?International journal of molecular sciences · 2026Review
- Characterization of rat serum amyloid A4 (SAA4): a novel member of the SAA superfamily.Biochemical and biophysical research communications · 2014Article
- Unraveling regulatory programs for NF-kappaB, p53 and microRNAs in head and neck squamous cell carcinoma.PloS one · 2013Article
- Zinc modulates the innate immune response in vivo to polymicrobial sepsis through regulation of NF-kappaB.American journal of physiology. Lung cellular and molecular physiology · 2010Article
- 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
- Two histone fold proteins, CHRAC-14 and CHRAC-16, are developmentally regulated subunits of chromatin accessibility complex (CHRAC).The EMBO journal · 2000Article
- C/EBPalpha is critical for the neonatal acute-phase response to inflammation.Molecular and cellular biology · 1998Article
- Regulation of serum amyloid A protein expression during the acute-phase response.The Biochemical journal · 1998Review
- A novel cis-acting element is essential for cytokine-mediated transcriptional induction of the serum amyloid A gene in nonhepatic cells.Molecular and cellular biology · 1996Article
- A compilation of composite regulatory elements affecting gene transcription in vertebrates.Nucleic acids research · 1995Article
- The effect of interleukin-1 on C-reactive protein expression in Hep3B cells is exerted at the transcriptional level.The Biochemical journal · 1995Article
- Promoter elements in the transcriptional activation of the human stromelysin-1 gene by the inflammatory cytokine, interleukin 1.The Biochemical journal · 1994Article
- YY1 represses rat serum amyloid A1 gene transcription and is antagonized by NF-kappa B during acute-phase response.Molecular and cellular biology · 1994Article
- Multiple forms of C/EBP beta bind the EFII enhancer sequence in the Rous sarcoma virus long terminal repeat.Molecular and cellular biology · 1994Article
- Induction of the mouse serum amyloid A3 gene by cytokines requires both C/EBP family proteins and a novel constitutive nuclear factor.Molecular and cellular biology · 1994Article
- Inflammation-associated amyloidogenesis. Lessons for Alzheimer's amyloidogenesis.Molecular neurobiology · 1994Review
- Transcription factors NF-IL6 and NF-kappa B synergistically activate transcription of the inflammatory cytokines, interleukin 6 and interleukin 8.Proceedings of the National Academy of Sciences of the United States of America · 1993Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Serum amyloid A (SAA) is a major acute-phase protein synthesized and secreted mainly by the liver. In response to inflammation, its expression is increased by 1000-fold, primarily because of a 200-fold increase in the rates of SAA gene transcription. We have shown that when 304 bp of 5' flanking region of the rat SAA1 gene is fused to a reporter gene, the chloramphenicol acetyltransferase (CAT) gene, CAT activity is induced in a cell-specific manner in response to conditioned media prepared from activated mixed lymphocyte cultures and recombinant interleukin-1. In this study, deletion of the SAA1 promoter to -120 bp with respect to the transcriptional start site did not diminish promoter activity; however, deletion to -94 bp renders the promoter completely inactive. Functional analysis have demonstrated that a 66-bp DNA fragment spanning -138 bp to -73 bp could confer cytokine responsiveness to a heterologous thymidine kinase promoter. Within this 66-bp responsive element resided an NF kappa B-like-binding site and a C/EBP-like-binding site. Although each binding site alone could confer responsiveness when stimulated with conditioned media and TPA, the response was much weaker than that observed when both sites were present. Moreover, site-specific mutations of either binding site completely abolished SAA1 promoter activity. Taken together, these results suggest a functional importance for and cooperative interaction of these two nuclear-factor binding sites in the cytokine-induced expression of the rat SAA1 gene.
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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.