[대학원 생명과학과 세미나 안내]

 

연사 : 이수영 교수(이화여자대학교 생명과학과)


연제 : Glycogen synthase kinase 3b in bone and the innate immune system

 

일시 : 2016년 9월 30일 (금오후 4

 

장소 하나과학관 A동 109


초청교수 : 고영규 교수


Abstract


Innate immune system is the first line barrier of host defense during pathogen infection and is also critical for effective adaptive immune system. Toll-like receptors (TLRs), highly conserved type I transmembrane pattern recognition receptors, are expressed on antigen presenting cells such as macrophages and dendritic cells. Tumor necrosis factor (TNF) receptor-associated factor 6 (TRAF6) is critical for the production of inflammatory cytokines in various TLR-mediated signaling pathways. However, it is poorly understood how TRAF6 regulates TLR3 responses. Here we demonstrate that GSK3b interacts with TRAF6 and positively regulates the TLR3-mediated signaling. Suppression of GSK3b expression or its kinase activity drastically reduces the production of inflammatory cytokines and the induction of c-Fos by decreasing extracellular signal-regulated kinase (ERK) and p38 phosphorylation. GSK3b physically associates with TRAF6 in a poly I:C-dependent manner. TRAF6 is determined to be a direct E3 ligase for GSK3b, and TRAF6-mediated GSK3b ubiquitination is essential for poly I:C-dependent cytokine production by promoting the TRIF-assembled signaling complex.