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.