Journal
SCIENCE SIGNALING
Volume 14, Issue 668, Pages -Publisher
AMER ASSOC ADVANCEMENT SCIENCE
DOI: 10.1126/scisignal.abc6178
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Funding
- National Health and Medical Research Council of Australia (NHMRC) [2002965, 1105023, 1142669, 1172929]
- IRIISS [9000653]
- Victorian State Government Operational Infrastructure Support
- CASS Foundation
- Australian Government Research Training Program Stipend Scholarship
- Wendy Dowsett Scholarship
- National Health and Medical Research Council of Australia [1142669, 2002965, 1105023] Funding Source: NHMRC
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Necroptosis is a lytic, proinflammatory cell death pathway that plays a role in host defense, but can contribute to the pathology of various diseases when dysregulated. The signaling chronology along the RIPK1-RIPK3-MLKL axis and the subcellular compartmentalization of signaling events are crucial for the initiation and execution of necroptosis. A network of modulators surrounding the necroptotic signaling core tunes necroptosis in a context-, cell type-, and species-dependent manner, making it a robust and emergency form of cell death.
Necroptosis is a lytic, proinflammatory cell death pathway, which has been implicated in host defense and, when dysregulated, the pathology of many human diseases. The central mediators of this pathway are the receptor-interacting serine/threonine protein kinases RIPK1 and RIPK3 and the terminal executioner, the pseudokinase mixed lineage kinase domain-like (MLKL). Here, we review the chronology of signaling along the RIPK1-RIPK3-MLKL axis and highlight how the subcellular compartmentalization of signaling events controls the initiation and execution of necroptosis. We propose that a network of modulators surrounds the necroptotic signaling core and that this network, rather than acting universally, tunes necroptosis in a context-, cell type-, and species-dependent manner. Such a high degree of mechanistic flexibility is likely an important property that helps necroptosis operate as a robust, emergency form of cell death.
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