TABLE 2

An overview on experimental observations that demonstrate an involvement of C / EBPs in the transcriptional regulation of several acute phase proteins (AP proteins)

AP Protein Cell Cultures Experimental Approach Agonistic TFs Antagonistic TFs C/EBP-Binding Authors
Factor VIII Human HepG2 cells LPS stimulation of cell culture, promotor deletion experiments with reporter gene assays C/EBP-β, NF-κB Begbie et al., 2000
α1-Acid-glycoprotein C/EBP-α, C/EBP-β Acute phase response element (APRE) Rabek and Papaconstantinou, 1999
α1-Acid-glycoprotein Rat livers LPS treatment of rats, nuclear extracts, gel shift assays 35 kDa C/EBP-β isoform Distal regulatory element (DRE) Petrovic et al., 1996
α1-Acid-glycoprotein Nucleolin Yang et al., 1994
α1-Acid-glycoprotein NF-κB and Nopp140 as coactivators for C/EBP-β via protein-protein interactions Lee et al., 1996
α1-Acid-glycoprotein Agonistic protein-protein interactions between C/EBP-β, Nopp140 and TFIIB Antagonistic protein-protein interactions between hnRNP and C/EBP-β, interruption of agonistic Nopp140/C/EBP-β interactions Miau et al., 1997, 1998
Serum amyloid A2 (SAA2) Co-operative protein-protein interaction of NF-κB p65 with C/EBP-β results in synergistic transcriptional activation of the SAA2 promotor Xia et al., 1997
LPS binding protein (LBP) Human hepatoma cell line IL-1β, IL-6, TNF-α and dexamethasone stimulation of cell culture, promotor deletion experiments with reporter gene assays AP-1, C/EBP-β Kirschning et al., 1997
Angiotensinogen NF-κB, C/EBP-β: both bind to overlapping nucleotides in a mutually exclusive manner C/EBP-β is a less potent transactivator than NF-κB Acute phase response element (APRE) in the multihormone-inducible enhancer nts −615 to −440 Brasier et al., 1994
Thrombin-activable fibrinolysis inhibitor (TAFI) Human HepG2 cells Promotor deletion experiments with reporter gene assays, gel mobility assays of nuclear extracts C/EBP-α, C/EBP-β, C/EBP-δ nts −53 to −40 Boffa et al., 2002
  • TF, transcription factor; nts, nucleotides numbered in relation to the start site of transcription within the respective promoter of the acute phase protein gene; agonistic TFs, transcription factors that enhance acute phase protein gene expression; antagonistic TFs, transcription factors that inhibit acute phase protein gene expression.