期刊
TRENDS IN BIOCHEMICAL SCIENCES
卷 44, 期 1, 页码 53-63出版社
ELSEVIER SCIENCE LONDON
DOI: 10.1016/j.tibs.2018.11.002
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资金
- National Health and Medical Research Council of Australia [1079700, 1105754, 1124735, 1124737, IRIISS 9000433]
The recent implication of the cell death pathway, necroptosis, in innate immunity and a range of human pathologies has led to intense interest in the underlying molecular mechanism. Unlike the better-understood apoptosis pathway, necroptosis is a caspase-independent pathway that leads to cell lysis and release of immunogens downstream of death receptor and Toll-like receptor (TLR) ligation. Here we review the role of recent structural studies of the core machinery of the pathway, the protein kinases receptor-interacting protein kinase (RIPK)1 and RIPK3, and the terminal effector, the pseudokinase mixed lineage kinase domain-like protein (MLKL), in shaping our mechanistic understanding of necroptotic signaling. Structural studies have played a key role in establishing models that describe MLKL's transition from a dormant monomer to a killer oligomer and revealing important interspecies differences.
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