NF‐κB activator Act1 associates with IL‐1/Toll pathway adaptor molecule TRAF6

FEBS Letters

Kai, Chikatoshi¹  Suzuki, Harukazu¹  Hayashizaki, Yoshihide¹  Kanamori, Mutsumi¹ 

[1] Laboratory for Genome Exploration Research Group, RIKEN Genomic Sciences Center (GSC), 1-7-22 Suehiro-cho, Tsurumi-ku, Yokohama 230-0045, Japan

关键词: Act1;    CIKS;    TRAF6;    Two-hybrid;    Protein–protein interaction;    NF-κB;    Act1;    NF-κB activator 1;    NF-κB;    nuclear factor kappa B;    CIKS;    connection to IKK and SAPK/JNK;    JNK;    c-Jun N-terminal kinase;    TRAF6;    tumor necrosis factor receptor-associated factor 6;    IKK;    IκB kinase;    IL-1;    interleukin-1;    MyD88;    protein encoded in myeloid differentiation gene 88;    Tollip;    Toll-interacting protein;    IRAK1;    interleukin-1 receptor-associated kinase 1;    TAB1;    transforming growth factor-β activated kinase 1 binding protein;    TAK1;    transforming growth factor-β activated kinase 1;    NIK;    NF-κB-inducing kinase;   

DOI  :  10.1016/S0014-5793(02)03688-8

学科分类：生物化学/生物物理

来源: John Wiley & Sons Ltd.

【 摘 要 】

NF-κB activator 1 (Act1), also called CIKS, is a recently identified protein with NF-κB and AP-1 activation activities through its association with the IκB kinase complex. We identified and confirmed that Act1 interacts with tumor necrosis factor receptor-associated factor 6 (TRAF6); notably, Act1 binds to TRAF6 only among TRAF family proteins. The amino-terminal half of Act1 is required for its interaction with the TRAF domain. Act1-mediated NF-κB activation was inhibited by a dominant-negative mutant of TRAF6 in a dose-dependent manner, and IL-1-induced NF-κB activation was inhibited by a high level of Act1 expression. Our results suggest that Act1 is involved in IL-1/Toll-mediated signaling through TRAF6.

【 授权许可】

Unknown