ArticleJournal of immunology (Baltimore, Md. : 1950)2007
A novel RBP-J kappa-dependent switch from C/EBP beta to C/EBP zeta at the C/EBP binding site on the C-reactive protein promoter.
Article in Journal of immunology (Baltimore, Md. : 1950), 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 16 citations in OpenAlex.
- IL-6 regulates induction of C-reactive protein gene expression by activating STAT3 isoforms.Molecular immunology · 2022Article
- Targeting C-Reactive Protein by Selective Apheresis in Humans: Pros and Cons.Journal of clinical medicine · 2022Review
- Reversible promoter methylation determines fluctuating expression of acute phase proteins.eLife · 2020Article
- Hepatocytes: a key cell type for innate immunity.Cellular & molecular immunology · 2016Review
- Deletion of RBP-J in dendritic cells compromises TLR-mediated DC activation accompanied by abnormal cytoskeleton reorganization.Molecular biology reports · 2013Article
- Oct-1 acts as a transcriptional repressor on the C-reactive protein promoter.Molecular immunology · 2012Article
- The protective function of human C-reactive protein in mouse models of Streptococcus pneumoniae infection.Endocrine, metabolic & immune disorders drug targets · 2008Review
- The connection between C-reactive protein and atherosclerosis.Annals of medicine · 2008Review
- Probing the phosphocholine-binding site of human C-reactive protein by site-directed mutagenesis.The Journal of biological chemistry · 1992Article
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3 authors at 1 institution in 1 country.
Funding
Abstract
Regulation of basal and cytokine (IL-6 and IL-1beta)-induced expression of C-reactive protein (CRP) in human hepatoma Hep3B cells occurs during transcription. A critical transcriptional regulatory element on the CRP promoter is a C/EBP binding site overlapping a NF-kappaB p50 binding site. In response to IL-6, C/EBPbeta and p50 occupy the C/EBP-p50 site on the CRP promoter. The aim of this study was to identify the transcription factors occupying the C/EBP-p50 site in the absence of C/EBPbeta. Accordingly, we treated Hep3B nuclear extract with a C/EBP-binding consensus oligonucleotide to generate an extract lacking active C/EBPbeta. Such treated nuclei contain only C/EBPzeta (also known as CHOP10 and GADD153) because the C/EBP-binding consensus oligonucleotide binds to all C/EBP family proteins except C/EBPzeta. EMSA using this extract revealed formation of a C/EBPzeta-containing complex at the C/EBP-p50 site on the CRP promoter. This complex also contained RBP-Jkappa, a transcription factor known to interact with kappaB sites. RBP-Jkappa was required for the formation of C/EBPzeta-containing complex. The RBP-Jkappa-dependent C/EBPzeta-containing complexes were formed at the C/EBP-p50 site on the CRP promoter in the nuclei of primary human hepatocytes also. In luciferase transactivation assays, overexpressed C/EBPzeta abolished both C/EBPbeta-induced and (IL-6 + IL-1beta)-induced CRP promoter-driven luciferase expression. These results indicate that under basal conditions, C/EBPzeta occupies the C/EBP site, an action that requires RBP-Jkappa. Under induced conditions, C/EBPzeta is replaced by C/EBPbeta and p50. We conclude that the switch between C/EBPbeta and C/EBPzeta participates in regulating CRP transcription. This process uses a novel phenomenon, that is, the incorporation of RBP-Jkappa into C/EBPzeta complexes solely to support the binding of C/EBPzeta to the C/EBP site.
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