FEBS Letters | |
p62 forms a ternary complex with PKCζ and PAR‐4 and antagonizes PAR‐4‐induced PKCζ inhibition | |
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;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
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