PMID:10588860

Citation	Estellés, A, Charlton, CA and Blau, HM (1999) The phosphoprotein protein PEA-15 inhibits Fas- but increases TNF-R1-mediated caspase-8 activity and apoptosis. Dev. Biol. 216:16-28
Abstract	We have characterized a phosphoprotein protein with a death effector domain that has a novel bifunctional role in programmed cell death. The 15-kDa phosphoprotein enriched in astrocytes (PEA-15) inhibits Fas-mediated apoptosis and increases tumor necrosis factor receptor-1 (TNF-R1)-mediated apoptosis in the same cell type in a ligand-dependent manner. Phosphorylation appears to play a role in its differential effects, since point mutations at one or both phosphorylation consensus sites within PEA-15 destroy its effect on Fas-mediated, but not TNF-R1-mediated, apoptosis. Furthermore, the differential effect is evident at the level of caspase-8 activity which is inhibited via Fas activation, but increased via TNF-R1 activation upon PEA-15 expression. These results show that PEA-15 provides a potential mechanism during development for distinguishing between diverse extracellular death-inducing signals that culminate either in apoptosis or in survival.
Links	PubMed Online version:10.1006/dbio.1999.9510
Keywords	3T3 Cells; Amino Acid Sequence; Animals; Antibodies/immunology; Antigens, CD95/immunology; Antigens, CD95/metabolism; Apoptosis/drug effects; Caspase 8; Caspase 9; Caspases/metabolism; Enzyme Activation/drug effects; Gene Expression; Mice; Molecular Sequence Data; Mutation; NF-kappa B/metabolism; Phosphoproteins/genetics; Phosphoproteins/pharmacology; Phosphorylation; Receptors, Tumor Necrosis Factor/metabolism; Signal Transduction; Tumor Necrosis Factor-alpha/pharmacology
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