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Receptor Interacting Protein Kinase 3 (RIPK3) is a key adaptor for programmed necrosis or necroptosis. Necroptosis is a non-apoptotic form of cell death that promotes inflammation through the release of endogenous “danger signals” from ruptured plasma membrane. RIPK3 interacts with other adaptors that contain the “RIP homotypic interaction motif” (RHIM) to form a tight complex that recruits downstream effectors for necroptosis. Although necroptosis is a major mechanism by which RIPK3 facilitates inflammation, recent evidence indicates that RIPK3 can also promote inflammation independent of necroptosis. Here, I will discuss the molecular mechanisms that govern necroptosis-dependent and independent signaling by RIPK3. Examples will be given to illustrate how the different RIPK3-dependent signaling responses orchestrate tissue homeostasis.