Induction of Apoptosis by Protein Inhibitor of Activated Stat1 through c-Jun NH2-terminal Kinase Activation
Copyright policy )Induction of Apoptosis by Protein Inhibitor of Activated Stat1 through c-Jun NH2-terminal Kinase Activation
Members of the protein inhibitor of activated signal transducer and activator of transcription (STAT) family (PIAS family) of proteins act as negative regulators of STATs in cytokine signaling. We report here that PIAS proteins have proapoptotic activity. PIAS1 induced apoptosis in both human 293T cells and human osteosarcoma U2OS cells. PIAS1 is localized in the nucleus as distinct nuclear dots. Ectopic expression of PIAS1 in U2OS cells activated JNK1 (c-Jun NH(2)-terminal kinase). A dominant-negative JNK1, capable of inhibiting PIAS1-induced JNK1 activation, blocked PIAS1-mediated apoptosis. Furthermore, a mutant PIAS1, lacking the first 9 amino acid residues, failed to repress Stat1-mediated gene activation although it retained its ability to activate JNK and to trigger apoptosis. Our results identify a novel function of PIAS1 in the induction of JNK-dependent apoptosis, independent of the previously known inhibitory activity of PIAS1 in STAT-mediated gene activation.
- University of California, Los Angeles United States
Cell Nucleus, Time Factors, Blotting, Western, JNK Mitogen-Activated Protein Kinases, Proteins, Apoptosis, Blotting, Northern, Protein Inhibitors of Activated STAT, Cell Line, Protein Structure, Tertiary, Enzyme Activation, Mice, Tumor Cells, Cultured, Animals, Humans, Mitogen-Activated Protein Kinases, Protein Binding, Signal Transduction
Cell Nucleus, Time Factors, Blotting, Western, JNK Mitogen-Activated Protein Kinases, Proteins, Apoptosis, Blotting, Northern, Protein Inhibitors of Activated STAT, Cell Line, Protein Structure, Tertiary, Enzyme Activation, Mice, Tumor Cells, Cultured, Animals, Humans, Mitogen-Activated Protein Kinases, Protein Binding, Signal Transduction
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