Necroptosis molecular mechanisms: recent findings regarding novel necroptosis regulators

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Necroptosis molecular mechanisms: recent findings regarding novel necroptosis regulators
Jinho Seo; Y W Nam; S Kim; Doo-Byoung Oh; J Song
Bibliographic Citation
Experimental and Molecular Medicine, vol. 53, no. 6, pp. 1007-1017
Publication Year
Necroptosis is a form of programmed necrosis that is mediated by various cytokines and pattern recognition receptors (PRRs). Cells dying by necroptosis show necrotic phenotypes, including swelling and membrane rupture, and release damage-associated molecular patterns (DAMPs), inflammatory cytokines, and chemokines, thereby mediating extreme inflammatory responses. Studies on gene knockout or necroptosis-specific inhibitor treatment in animal models have provided extensive evidence regarding the important roles of necroptosis in inflammatory diseases. The necroptosis signaling pathway is primarily modulated by activation of receptor-interacting protein kinase 3 (RIPK3), which phosphorylates mixed-lineage kinase domain-like protein (MLKL), mediating MLKL oligomerization. In the necroptosis process, these proteins are fine-tuned by posttranslational regulation via phosphorylation, ubiquitination, glycosylation, and protein-protein interactions. Herein, we review recent findings on the molecular regulatory mechanisms of necroptosis.
Springer-Nature Pub Group
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Aging Convergence Research Center > 1. Journal Articles
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