http://chineseinput.net/에서 pinyin(병음)방식으로 중국어를 변환할 수 있습니다.
변환된 중국어를 복사하여 사용하시면 됩니다.
( Jia Yi Yu ),( Xiao Fei Zhou ),( Mi Kyoung Chang ),( Mako Nakaya ),( Jae Hoon Chang ),( Yi Chuan Xiao ),( J. William Lindsey ),( Stephanie Dorta Estremera ),( Wei Cao ),( Anna Zal ),( Tomasz Zal ),( 영남대학교 약품개발연구소 2015 영남대학교 약품개발연구소 연구업적집 Vol.25 No.-
Development of an immune or autoimmune response involves T-cell activation in lymphoid organs and subsequent migration to peripheral tissues. Here we show that T-cell-specific ablation of the kinase TBK1 promotes T-cell activation but causes retention of effector T cells in the draininglumph node in a neuroinflammatory autoimmunity model,experimental autoimmune encephalomyelitis (EAE).Atolder ager,the T-cell-conditional TBK1-knockout mice also spontaneously accumulate T cells with activated phenotype.TBK1 contrlos the activation of AKT and its downsream kinase m TIORC1 by a mechanism involving TBK1-stimulated AKT ubiquitination and degradation. The deregulated AKT-mTORC1 signalling in turn contributes to enhanced T-cell activation and impaired effector T-cell egress from draining lymph nodes. Treatment of mice with a small-molecule inhibitor fo TBK1 inhibits EAE induction. These results suggest a role for TBK1 in regulating T-cell migration and establish TBK1 as a regulator of the AKT-mTORC1 signalling axis.