Role of caspases in TNF-mediated regulation of cPLA2
Role of caspases in TNF-mediated regulation of cPLA2
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DOI：
10.1016/s0014-5793(02)03407-5
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发表时间：
2002-10-30
期刊：
影响因子：
3.5
通讯作者：
Adam-Klages, S
中科院分区：
文献类型：
--
作者：
Krönke, M;Adam-Klages, S
肿瘤坏死因子（TNF）的促炎活性主要是由胞质磷脂酶A(2) （cPLA(2)）产生花生四烯酸，花生四烯酸是白三烯和前列腺素的前体。cPLA(2)的激活和促炎脂质介质的诱导与细胞凋亡的目的意义形成鲜明对比，细胞凋亡是为了避免炎症反应。在这篇综述中，我们强调了caspase介导的cPLA(2)的裂解和失活的证据，这似乎是TNF在细胞凋亡中下调cPLA(2)活性的重要机制。(C) 2002年欧洲生化学会联合会。Elsevier Science B.V.版权所有。
A major part of the proinflammatory activity of tumor necrosis factor (TNF) is brought about by cytosolic phospholipase A(2) (cPLA(2)) that generates arachidonic acid, the precursor for the production of leukotrienes and prostaglandins. The activation of cPLA(2) 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 cPLA(2), which seems to be an important mechanism by which TNF downregulates cPLA(2) activity in cells undergoing apoptosis.(C) 2002 Federation of European Biochemical Societies. Published by Elsevier Science B.V. All rights reserved.