坏死性下垂
炎症体
串扰
细胞生物学
程序性细胞死亡
裂谷1
信号转导
生物
炎症
受体
细胞凋亡
免疫学
工程类
遗传学
电子工程
作者
Soo Jung Cho,Alexander Pronko,Heather Stout‐Delgado
出处
期刊:Elsevier eBooks
[Elsevier]
日期:2022-11-29
卷期号:: 499-510
被引量:1
标识
DOI:10.1016/b978-0-323-91802-2.00034-7
摘要
Necroptosis is a regulated form of cell death, with hallmark features of both apoptosis and necrosis. Necroptosis is an effective means of caspase-independent cell death and can play an important role in limiting the time in which pathogenic stimuli can inhabit the cell. Necroptosis can be stimulated by toll-like receptors, death receptors, and other mediators. Recent studies have demonstrated that receptor-interacting protein kinase 3, a key protein in necroptosis, can directly activate the inflammasome. In this chapter, we will focus on the molecular mechanisms that underlie necroptotic signaling and how crosstalk between this pathway and the inflammasome can contribute to inflammation.
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