Role of caspases in TNF‐mediated regulation of cPLA2

FEBS Letters

Adam-Klages, Sabine¹  Krönke, Martin² 

[1] Institute of Immunology, Medical Center, University of Kiel, Kiel, Germany;Institute for Medical Microbiology, Immunology, and Hygiene, Medical Center, University of Cologne, Goldenfelsstr. 19–21, 50935 Cologne, Germany

关键词: Cytosolic phospholipase A2;    Tumor necrosis factor;    Death domain;    Caspase;    cPLA2;    cytosolic phospholipase A2;    DD;    death domain;    ERK;    extracellular signal-regulated kinase;    SMase;    sphingomyelinase;    TNF;    tumor necrosis factor;    TNFR1;    p55 TNF receptor type 1;   

DOI  :  10.1016/S0014-5793(02)03407-5

学科分类：生物化学/生物物理

来源: John Wiley & Sons Ltd.

【 摘 要 】

A major part of the proinflammatory activity of tumor necrosis factor (TNF) is brought about by cytosolic phospholipase A₂ (cPLA₂) that generates arachidonic acid, the precursor for the production of leukotrienes and prostaglandins. The activation of cPLA₂ and induction of proinflammatory lipid mediators is in striking contrast to the teleologic meaning of apoptosis, which is to avoid an inflammatory reaction. In this review we highlight the evidence for a caspase-mediated cleavage and inactivation of cPLA₂, which seems to be an important mechanism by which TNF downregulates cPLA₂ activity in cells undergoing apoptosis.

【 授权许可】

Unknown