Regulation of inflammasomes by ubiquitination

被引:63
作者
Bednash, Joseph S. [1 ]
Mallampalli, Rama K. [1 ,2 ,3 ]
机构
[1] Univ Pittsburgh, Dept Med, Acute Lung Injury Ctr Excellence, Div Pulm Allergy & Crit Care Med, 930 Scaife Hall, Pittsburgh, PA 15213 USA
[2] Univ Pittsburgh, Dept Cell Biol & Physiol & Bioengn, Pittsburgh, PA 15213 USA
[3] Vet Affairs Pittsburgh Healthcare Syst, Med Specialty Serv Line, Pittsburgh, PA 15240 USA
关键词
deubiquitinase; E3; ligase; inflammasome; innate immunity; ubiqutin; NF-KAPPA-B; NLRP3; INFLAMMASOME; CUTTING EDGE; CELL-DEATH; ACTIVATION; PROTEASOME; IL-1-BETA; LIPOPOLYSACCHARIDE; RECOGNITION; MECHANISM;
D O I
10.1038/cmi.2016.15
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
Inflammasomes are multi-protein complexes that regulate the innate immune response by facilitating the release of inflammatory cytokines in response to pathogen exposure or cellular damage. Pro-inflammatory inflammasome signaling is vital to host defense and helps initiate the process of tissue repair following an insult to the host, but can be injurious, when excessive or chronic. As such, inflammasome activity is tightly regulated. Here we discuss one critical mechanism of inflammasome regulation, ubiquitination, that functions as a universal modulator of protein stability and trafficking. Recent studies have provided important insights into the regulation of inflammasome activation by protein ubiquitination. We review the molecular regulation of inflammasome function, specifically, as it relates to ubiquitination, and discuss the implications for the development of therapeutics to specifically target aberrant inflammasome signaling.
引用
收藏
页码:722 / 728
页数:7
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