期刊
IMMUNOLOGICAL REVIEWS
卷 246, 期 -, 页码 107-124出版社
WILEY
DOI: 10.1111/j.1600-065X.2012.01100.x
关键词
deubiquitinases; NF-?B; A20; CYLD; inflammation
类别
资金
- NIH [P01CA128115, R01CA135362, R01GM083143]
The nuclear factor-?B (NF-?B) pathway is a critical regulator of innate and adaptive immunity. Noncanonical K63-linked polyubiquitination plays a key regulatory role in NF-?B signaling pathways by functioning as a scaffold to recruit kinase complexes containing ubiquitin-binding domains. Ubiquitination is balanced by deubiquitinases that cleave polyubiquitin chains and oppose the function of E3 ubiquitin ligases. Deubiquitinases therefore play an important role in the termination of NF-?B signaling and the resolution of inflammation. In this review, we focus on NF-?B regulation by deubiquitinases with an emphasis on A20 and CYLD. Deubiquitinases and the ubiquitin/proteasome components that regulate NF-?B may serve as novel therapeutic targets for inflammatory diseases and cancer.
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