p62 forms a ternary complex with PKCζ and PAR‐4 and antagonizes PAR‐4‐induced PKCζ inhibition

FEBS Letters

Chang, Suhwan¹  Kim, Jung Hoe²  Shin, Jaekyoon¹ 

[1]Sungkyunkwan University, School of Medicine and Samsung Biomedical Research Institute, 300 ChunChun-Dong, Jangan-Gu, Suwon, Kyonggi-Do, South Korea

[2]Department of Biological Science, Korea Advanced Institute of Sciences and Technology, Taejon, South Korea

关键词: p62;    Prostate apoptosis response-4;    Protein kinase Cζ;    Nuclear factor κB;    Ternary complex;    Apoptosis;    RIP;    receptor interacting protein;    TNF;    tumor necrosis factor;    TRAF;    tumor necrosis factor receptor associated factor;    PKC;    protein kinase C;    PAR-4;    prostate apoptosis response-4;    IKKβ;    IκB kinase β;    NFκB;    nuclear factor κB;   

DOI  :  10.1016/S0014-5793(01)03224-0

学科分类：生物化学/生物物理

来源: John Wiley & Sons Ltd.

【 摘 要 】

It has been reported that prostate apoptosis response-4 (PAR-4) binds to and inhibits protein kinase Cζ (PKCζ) which phosphorylates IκB kinase β (IKKβ) for nuclear factor κB (NFκB) activation, while p62 binds to and recruits PKCζ to the NFκB signaling complex. Thus, a mechanism to coordinate the two binding proteins for the regulation of PKCζ is expected to exist. The present data show that p62 and PAR-4 do not compete for PKCζ binding but directly interact each other and form a ternary complex with PKCζ. Furthermore, p62 not only enhances the catalytic activity of PKCζ but also reactivates catalytically inactive PAR-4-bound PKCζ. As the result, over-expression of p62 protects cells from PAR-4-mediated inactivation of NFκB and apoptotic death. Thus, the regulatory role of p62 for free and PAR-4-bound PKCζ is important in activation of NFκB.

【 授权许可】

Unknown