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论文题目: HECTD3 Mediates TRAF3 Polyubiquitination and Type I Interferon Induction During Bacterial Infection
作者: Li F, Li Y, Liang H, Xu T, Kong Y, Huang M, Xiao J, Chen X, Xia H, Wu Y, Zhou Z, Guo X, Hu C, Yang C, Cheng X, Chen C, Qi X.
联系作者: qixiaopeng@mail.kiz.ac.cn
发表年度: 2018
DOI: doi: 10.1172/JCI120406
摘要:

Lysine-63 (K63)-linked polyubiquitination of TRAF3 coordinates the engagement of pattern recognition receptors to recruited adaptor proteins and downstream activator TBK1 in pathways that induce type I interferon (IFN). Whether auto-ubiquitination or other E3 ligases mediate K63-linked TRAF3 polyubiquitination remains unclear. We demonstrated that mice deficient in E3 ligase gene Hectd3remarkably increased host defense against infection by intracellular bacteria F. novicida, Mycobacterium, and Listeria by limiting bacterial dissemination. In the absence of HECTD3, type I IFN response was impaired during bacterial infection both in vivo and in vitro. HECTD3 regulated type I IFN production by mediating K63-linked polyubiquitination of TRAF3 at residue K138. The catalytic domain of HECTD3 regulated TRAF3 K63 polyubiquitination, which enabled TRAF3-TBK1 complex formation. Our study offers novel insights into mechanisms of TRAF3 modulation and provides potential therapeutic targets against infections by intracellular bacteria and inflammatory diseases

刊物名称: Journal of Clinical Investigation
论文出处: https://www.jci.org/articles/view/120406
影响因子: 12.784(2016年)