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PMID:11684016
| Citation |
Buck, M, Poli, V, Hunter, T and Chojkier, M (2001) C/EBPbeta phosphorylation by RSK creates a functional XEXD caspase inhibitory box critical for cell survival. Mol. Cell 8:807-16 |
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| Abstract |
Upon activation by liver injury, hepatic stellate cells produce excessive fibrous tissue leading to cirrhosis. The hepatotoxin CCl(4) induced activation of RSK, phosphorylation of C/EBPbeta on Thr(217), and proliferation of stellate cells in normal mice, but caused apoptosis of these cells in C/EBPbeta-/- or C/EBPbeta-Ala(217) (a dominant-negative nonphosphorylatable mutant) transgenic mice. Both C/EBPbeta-PThr(217) and the phosphorylation mimic C/EBPbeta-Glu(217), but not C/EBPbeta-Ala(217), were associated with procaspases 1 and 8 in vivo and in vitro and inhibited their activation. Our data suggest that C/EBPbeta phosphorylation on Thr(217) creates a functional XEXD caspase substrate/inhibitor box (K-Phospho-T(217)VD) that is mimicked by C/EBPbeta-Glu(217) (KE(217)VD). C/EBPbeta-/- and C/EBPbeta-Ala(217) stellate cells were rescued from apoptosis by the cell permeant KE(217)VD tetrapeptide or C/EBPbeta-Glu(217). |
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| Keywords |
Acetylcysteine/analogs & derivatives; Acetylcysteine/pharmacology; Amino Acid Motifs; Animals; Apoptosis/physiology; CCAAT-Enhancer-Binding Protein-beta/genetics; CCAAT-Enhancer-Binding Protein-beta/metabolism; Carbon Tetrachloride/toxicity; Caspases/antagonists & inhibitors; Caspases/metabolism; Cell Survival/physiology; Cells, Cultured; Culture Media, Serum-Free; Enzyme Activation; Enzyme Precursors/metabolism; Hepatocytes/cytology; Hepatocytes/drug effects; Hepatocytes/physiology; Humans; Liver Cirrhosis, Experimental/chemically induced; Male; Mice; Mice, Transgenic; Microscopy, Confocal; Phosphorylation; Rats; Recombinant Proteins/genetics; Recombinant Proteins/metabolism; Ribosomal Protein S6 Kinases/genetics; Ribosomal Protein S6 Kinases/metabolism |
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Significance
Annotations
| Gene product | Qualifier | GO ID | GO term name | Evidence Code | with/from | Aspect | Notes | Status |
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See also
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