坏死性下垂
裂谷1
促炎细胞因子
程序性细胞死亡
肿瘤坏死因子α
炎症
细胞生物学
下调和上调
癌症研究
NF-κB
细胞凋亡
生物
免疫学
生物化学
基因
作者
Adrian T. Ting,Mathieu J.M. Bertrand
标识
DOI:10.1016/j.it.2016.06.002
摘要
TNF is a master proinflammatory cytokine whose pathogenic role in inflammatory disorders has long been attributed to induction of proinflammatory mediators. TNF also activates cell survival and death pathways, and recent studies demonstrated that TNF also causes inflammation by inducing cell death. The default response of most cells to TNF is survival and NF-κB-mediated upregulation of prosurvival molecules is a well-documented protective mechanism downstream of TNFR1. Recent studies revealed the existence of an NF-κB-independent cell death checkpoint that restricts cell demise by inactivating RIPK1. Disruption of this checkpoint leads to RIPK1 kinase-dependent death and causes inflammation in vivo. These revelations bring complexity to the control of TNF-induced cell death, and suggest clinical benefit of RIPK1 inhibitors in TNF-driven human inflammatory disorders.
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