Caspase 8 inhibits programmed necrosis by processing CYLD (original) (raw)
References
Brenner, D. & Mak, T. W. Mitochondrial cell death effectors. Curr. Opin. Cell Biol.21, 871–877 (2009). ArticleCAS Google Scholar
Chan, F. K. et al. A role for tumor necrosis factor receptor-2 and receptor-interacting protein in programmed necrosis and antiviral responses. J. Biol. Chem.278, 51613–51621 (2003). ArticleCAS Google Scholar
Degterev, A. et al. Chemical inhibitor of nonapoptotic cell death with therapeutic potential for ischemic brain injury. Nat. Chem. Biol.1, 112–119 (2005). ArticleCAS Google Scholar
Cho, Y. S. et al. Phosphorylation-driven assembly of the RIP1-RIP3 complex regulates programmed necrosis and virus-induced inflammation. Cell137, 1112–1123 (2009). ArticleCAS Google Scholar
He, S. et al. Receptor interacting protein kinase-3 determines cellular necrotic response to TNF-α. Cell137, 1100–1111 (2009). ArticleCAS Google Scholar
Zhang, D. W. et al. RIP3, an energy metabolism regulator that switches TNF-induced cell death from apoptosis to necrosis. Science325, 332–336 (2009). ArticleCAS Google Scholar
Oberst, A. et al. Catalytic activity of the caspase-8-FLIP(L) complex inhibits RIPK3-dependent necrosis. Nature471, 363–367 (2011). ArticleCAS Google Scholar
Ch’en, I. L., Tsau, J. S., Molkentin, J. D., Komatsu, M. & Hedrick, S. M. Mechanisms of necroptosis in T cells. J. Exp. Med.208, 633–641 (2011). Article Google Scholar
Zhang, H. et al. Functional complementation between FADD and RIP1 in embryos and lymphocytes. Nature471, 373–376 (2011). ArticleCAS Google Scholar
Kang, T. B. et al. Mutation of a self-processing site in caspase-8 compromises its apoptotic but not its nonapoptotic functions in bacterial artificial chromosome-transgenic mice. J. Immunol.181, 2522–2532 (2008). ArticleCAS Google Scholar
Hitomi, J. et al. Identification of a molecular signaling network that regulates a cellular necrotic cell death pathway. Cell135, 1311–1323 (2008). ArticleCAS Google Scholar
Li, M. & Beg, A. A. Induction of necrotic-like cell death by tumor necrosis factor alpha and caspase inhibitors: novel mechanism for killing virus-infected cells. J. Virol.74, 7470–7477 (2000). ArticleCAS Google Scholar
Wang, L., Du, F. & Wang, X. TNF-α induces two distinct caspase-8 activation pathways. Cell133, 693–703 (2008). ArticleCAS Google Scholar
He, K. L. & Ting, A. T. Essential role for IKKγ/NEMO in TCR-induced IL-2 expression in Jurkat T cells. Eur. J. Immunol.33, 1917–1924 (2003). ArticleCAS Google Scholar
Wolf, B. B., Schuler, M., Echeverri, F. & Green, D. R. Caspase-3 is the primary activator of apoptotic DNA fragmentation via DNA fragmentation factor-45/inhibitor of caspase-activated DNase inactivation. J. Biol. Chem.274, 30651–30656 (1999). ArticleCAS Google Scholar
Holler, N. et al. Fas triggers an alternative, caspase-8-independent cell death pathway using the kinase RIP as effector molecule. Nat. Immunol.1, 489–495 (2000). ArticleCAS Google Scholar
Degterev, A. et al. Identification of RIP1 kinase as a specific cellular target of necrostatins. Nat. Chem. Biol.4, 313–321 (2008). ArticleCAS Google Scholar
Wright, A. et al. Regulation of early wave of germ cell apoptosis and spermatogenesis by deubiquitinating enzyme CYLD. Dev. Cell13, 705–716 (2007). ArticleCAS Google Scholar
Ea, C. K., Deng, L., Xia, Z. P., Pineda, G. & Chen, Z. J. Activation of IKK by TNFα requires site-specific ubiquitination of RIP1 and polyubiquitin binding by NEMO. Mol. Cell22, 245–257 (2006). ArticleCAS Google Scholar
Wu, C. J., Conze, D. B., Li, T., Srinivasula, S. M. & Ashwell, J. D. Sensing of Lys 63-linked polyubiquitination by NEMO is a key event in NF-κB activation. Nat. Cell Biol.8, 398–406 (2006). ArticleCAS Google Scholar
O’Donnell, M. A., Legarda, D., Skountzos, P., Yeh, W. C. & Ting, A. T. Ubiquitination of RIP1 regulates an NF-κB-independent cell-death switch in TNF signaling. Curr. Biol.17, 418–424 (2007). Article Google Scholar
Legarda-Addison, D., Hase, H., O’Donnell, M. A. & Ting, A. T. NEMO/IKK_γ_ regulates an early NF-κB-independent cell-death checkpoint during TNF signaling. Cell Death Differ.16, 1279–1288 (2009). ArticleCAS Google Scholar
O’Donnell, M. A. & Ting, A. T. Chronicles of a death foretold: Dual sequential cell death checkpoints in TNF signaling. Cell Cycle9, 1065–1071 (2010). Article Google Scholar
O’Donnell, M. A. & Ting, A. T. RIP1 comes back to life as a cell death regulator in TNFR1 signaling. FEBS J.278, 877–887 (2011). Article Google Scholar
Massoumi, R., Chmielarska, K., Hennecke, K., Pfeifer, A. & Fassler, R. Cyld inhibits tumor cell proliferation by blocking Bcl-3-dependent NF-κB signaling. Cell125, 665–677 (2006). ArticleCAS Google Scholar
Peters, M. E. Programmed cell death: Apoptosis meets necrosis. Nature471, 310–312 (2011). Article Google Scholar
Brouckaert, G. et al. Phagocytosis of necrotic cells by macrophages is phosphatidylserine dependent and does not induce inflammatory cytokine production. Mol. Biol. Cell15, 1089–1100 (2004). ArticleCAS Google Scholar
Hirt, U. A. & Leist, M. Rapid, noninflammatory and PS-dependent phagocytic clearance of necrotic cells. Cell Death Differ.10, 1156–1164 (2003). ArticleCAS Google Scholar
van Delft, M. F., Smith, D. P., Lahoud, M. H., Huang, D. C. & Adams, J. M. Apoptosis and non-inflammatory phagocytosis can be induced by mitochondrial damage without caspases. Cell Death Differ.17, 821–832 (2010). ArticleCAS Google Scholar
Waring, P., Lambert, D., Sjaarda, A., Hurne, A. & Beaver, J. Increased cell surface exposure of phosphatidylserine on propidium iodide negative thymocytes undergoing death by necrosis. Cell Death Differ.6, 624–637 (1999). ArticleCAS Google Scholar
Friedman, C. S. et al. The tumour suppressor CYLD is a negative regulator of RIG-I-mediated antiviral response. EMBO Rep.9, 930–936 (2008). ArticleCAS Google Scholar
Su, A. I. et al. A gene atlas of the mouse and human protein-encoding transcriptomes. Proc. Natl Acad. Sci. USA101, 6062–6067 (2004). ArticleCAS Google Scholar
Saldanha, A. J. Java Treeview-extensible visualization of microarray data. Bioinformatics20, 3246–3248 (2004). ArticleCAS Google Scholar